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482 Cards in this Set

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Arm of the immune system:
Barriers: Anatomic, Physiologic, Phagocytic (monocytes, neutrophils, macrophages), Inflammatory events
Innate Immune System
Arm of immune system that present intrinsically, nonspecific, no memory, and limited diversity
Innate Immune System
Arm of the immune system:
Lymphocytes (T & B cells) and plasma cells (end cells of B-lymphocyte differentiation); Antigen Presenting Cells (macrophages, B cells, dendritic cells)
Adaptive Immune System
Arm of immune system that is inducible, specific, has memory, extensive diversity, self versus non-self distinction, self-limiting
Adaptive Immune System
antibodies produced by B lymphocytes bind to pathogens and assit w/ phagocytosis
What activates complement
Antibodies produced by plasma cells bind to pathogen and activation copmlement
Gram Stain
"Im positively BLUE over you!"
Gram-positive = BLUE
Gram Stain
"No (negative) RED commies!!"
Gram-negative = RED
6 Classic Gram (+) bacteria
2 cocci, 4 bacilli
(1) Streptococci (strips)
(2) Staphylcocci (clusters)
2 Spore-forming bacilli
(3) Bacillus
(4) Clostridium
2 Bacilli
(5) Corynebacterium
(6) Listeria
Only Gram (-) cocci
diplococcus (looks like 2 coffee beans kissing)
Only spirial shaped Gram (-) organisms
Spirochetes: Treponema, Borrelia, Leptospira
Bacterial organism that does not have a cell wall
Mycoplasma, have a simple cell membrane
Gram (+) Organisms with branching filamentous growth
Actinomyces (anaerobic)
Nocardia (partially acid-fast)
Gram (-) Rods
Enterics (E. coli, Shigella, Salmonella, Yersinia, Klebsiella, Proteus, Enterobacter, Serratia, Vibrio, Campylobacter, Helicobacter, Pseudomonas, Bacteroids)
Pleomorphic Gram (-) organisms
Gram (+) and Gram (-) Oligate Aerobes
Use glycolysis, TCA cycle, & electron transport chain w/ O2 as final electron acceptor, have catalase, peroxidase, superoxide dismutase
Gram (+): Nocardia, Bacillus cereus
Gram (-): Neisseria, Pseudomonas, Bordetella, Legionalla, Brucella
Acid-Fast: Mycobacterium
Gram (+) and Gram (-) Facultative Anaerobes
Aerobic, use O2 as an electron acceptor in their electron transfer chain, have catalase & superoxide dismutase, CAN grow in absence of oxygen using fermentation for energy
Gram (+): Staphylcoccus, Bacillus anthracis, Corynebacterium, Listeria, Actinomyces
Gram (-): Most gram (-) rods
Gram (+) and Gram (-) Microaerophilic
Use fermentation as energy & have no electron transport system, can tolerate low levels of O2 b/c they have superoxide dismutase (no catalase)
Gram (+): Streptococcus (some spp are facultative anaerobes)
Gram (-): Spirochetes (Treponema, Boerrelia, Leptospira), Campylobacter
Gram (+) and Gram (-) Oligate Abaerobes
Fermentation for energy, no enzymes to break down Oxygen
Gram (+): Clostridium
Gram (-): Bacteroides
all medically important bacteria, use chemical & organic compounds, such as glucose for energy
Obligate intracelluar organisms
not capable of the metabolic pathways for ATP syn & must steal ATP from their host, they live in their host cell & can't survive w/o a host --> Energy Parasites
Ex: Chlamydia, Rickettsia
Facultative intracelluar organisms
bacteria that are phagocytosed by host's macphs & neutrophils & survive w/in the WBCs unharmed, they inhibit phagosome-lysosome fusion, thus escaping hydrogen peroxide & superoxide radicals
Ex: Listeria monocytogenes, Slamonella typhi, Yersinia, Francisella turlarensis, Brucella, Legionella, Mycobacterium
Endotoxins are only present in Gram (-) bacteria w/ one exception
Listeria monocytogenes

Endotoxin is a piece of the outer membrane lipopolysaccharide (LPS), Lipid A
Where do all cells from the immune system arise from
Pluripotent stem cell
What signal to the pluripotent stem cell causes it to differentiate into the Lymphoid stem cell & what will it make
Makes NK Cells, B-cells, T-cells
Lymphoid cells (except NK cells) are in the adaptive branch)
What signal to the pluripotent stem cell causes it to differentiate into the Myeloid stem cell & what will it make
Makes RBCs, Platelets, Basophils, Mast cells, Eosinophils, Neutrophils, Monocytes, Macrophages, & Dendritic Cells
-Myeloid cells are in the innate branch
What are the signals for myeloid stem cell to differentiate into Eosinophil progenitor, Megakaryocyte, & Erythroid Progenitor
Myeloid Progenitor:
IL-5 --> Eosinophil progenitor: IL-5 --> Eosinophil
Thrombopoietin --> Megakaryocyte --> IL-11 --> Platelets
Erythropoietin --> Erythroid Progenitor --> Erythrocyte
What myeloid cell is found in the bloodstrem, kidney bean-shaped nucleus, CD14 (+), is phagocytic & differentiates into tissue macrophages
What myeloid cell is found in tissues, has a ruffled membrane, cytoplasm w/ vacuoles & vesicles, CD14 (+), performs phagocytosis & secretes cytokines
What myeloid cell is found in the Epithelia & tissues, has long cytoplasmic arms, functions include antigen capture, transport, & presentation
Dendritic Cell
What myeloid cell is found in the bloodstrem, has a multi-lobed nucleus & small pink granules, performs phagocytosis & activation of bactericidal mechanisms
What myeloid cell is found in the bloodstrem, bilobed nucleus & large pink granules, & acts to kill antibody-coated parasites
Lymphoid cell found in the bloodstream, lymph nodes, spleen, submucosa & epithelim, large, dark nucles w/ small rim of cytoplasm
B cells, T cells
CD19, CD20, CD21 (+) & produces antibody
CD3, CD4 (+), helps regulate immune responses
T helper cells
CD3, CD8 (+), kill altered or infected cells
Cytotoxic T cells
Lymphoid cell found in the bloodstream, large cytoplasmic granules, CD16, CD56 (+) & what is it's fcn
Natural Killer Lymphocyte: kills tumor/virus cell targets or antibody coated target cells
Lymphoid cell found lymph nodes, spleen, mucosal-associated lymphoid tissues, and bone marrow, small dark nucleus, intensely staining golgi apparatus
Plasma Cell
End cell of B-cell differentiationm produce antibody
Plasma Cell
Myeloid cell found in the bloodstream, has a bilobed nucleus w/ large blue granules, it is nonphagocytic & releases pharmacologically active substances during allergic responses
Myeloid cell found in tissues, mucosa, & epithelia, has a small nucleus & cytoplasm is packed with large blue granules, releases granules containing histamine, etc. during allergic responses
Mast Cell
When is a mature B lymphocyte classified as a Naive B-cell
when it has not yet come in contact with antigen
What are the naive B-cell antigen receptors
IgM and IgD
What are the naive T-cell antigen receptors
T-cell receptor (TCR) made of alpha and beta chains
What makes up the antigen receptor of the B lymphocyte
Membrane-bound Immunoglobulin, has a 4-chain glycoprotein molecule that serves as the basic monomeric unit for each of the distinct Ab molecules, has two identical halves, each componsed of a long, Heavy chain (mu for IgM, delta for IgD) & a shorter, light chain (kappa or lambda), a "hinge" region joins the heavy chains
What does the variable region on the N-terminus of heavy and light chains determine
Idiotype = antigen specificity
What does the constant region on the C-terminus of heavy and light chains determine
Isotype = class of Ig which determines what you are going to do w/ the Ag bound in terms of function and biological effects
What lymphocyte cells recognize unprocessed antigens & which cell recognizes cell-bound peptides
B-Cell: unprocessed antigens
T-Cell: cell-bound peptides
What is the B-cell signal transduction complex composed of
Heterodimer of Ig-alpha & Ig-beta on each side of the receptor, and CD19 & CD21 co-receptors (lower threshold of Ags)
What is the T-cell signal transduction complex composed of
multichain structure called CD3
Membrane Marker for B-cells
CD19, CD20, CD21
membran marker for T-cells (T helper & cytotoxic T cells)
How are heavy chain variable domains of antigen receptors produced
B-lymphocyte progenitors select randomly & in the absence of stimulating antigen to recombine 3 gene segments, designated variable (V), diversity (D), & joining (J) to produce unique sequences of amino acids in the variable domains (VDJ recombination)
How are light chain variable domains of antigen receptors produced
B-lymphocyte progenitor preforms random rearrangement of two types of gene segments (V & J) to encode the variable dome of LC
-mRNA molecules are created which joins this variable domain sequence to mu or delta constant domains
What is the fcn of terminal deoxyribonucleotidyl transferase (Tdt)
while HC segments are undergoing recombination, this enzyme randomly inserts bases (w/o a template on the complementary strand) at the jcns of V, D, & J segments)
-not active during light chain rearrangement
What is N-nucleotide addition
When Terminal deoxyribonucleotidyl transferase (Tdt) enzyme randomly inserts bases (w/o a template on the complementary strand) at the jcns of V, D, & J segments)
How many chances does a cell have to produce a functional heavy (or beta) chain
(1) VJD rearrangments
(2) rearranging gene segments of the homologous chromosome
-if it fails to make a functional protein from the rearrangement of segments on either chrom the cell undergoes apoptosis
Allelic Exclusion
Once a functional product has been acheived by one of these rearrangements the cell shuts off the rearrangement and expression of the other allele on the homologous chromosome
--> process ensures that B & T lymphocytes synthesize only one specific antigen-receptor per cell
What is used as a marker for early stage T- & B- cell development in Acute Lymphoblastic Leukemia
What is the first set of constant domains for the heavy chain of Ig that is transcribed
IgM, then IgD
Omenn Syndrome (clinical outcome of failed gene rearrangment)
AR, missense mutation in rag genes, causing rag enzymes to only have partial activity
-Lack of B cells (below limits of detection)
-Marked decrease in T cells
-Characterized by early onset, failure to thrive, red rash (generalized), diarrhea, & severe immune deficiency
Severe Combined Immunodeficiency (SCID), (clinical outcome of failed gene rearrangment)
AR, Nill mutations in rag1 or rag2 genes, no rag enzyme activity
-Total lack of B and T cells
-Total defects in humoral & cell-mediated immunity
What and where are the primary lymphoid organs
Sites of lymphoid-cell development (lymphopoieisis)
-Bone Marrow
What and where are the seconary lymphoid organs
Sites of antigen exposure
-Lymph nodes
-Mucosal-associated lymphoid tissues
What do cells whose idiotype has too great an affinity for normal cellular molecules undergo in the bone marrow and the peripherhy
Bone marrow: Clonal Deltion
Peripherhy: Clonal Anergy
What T-cells are allowed to leave the bone marrow
T-cells that are selectively unresponsive to self-antigens (tolerant)
What does the outer cortex & Inner medulla of the thymus contain
Outer cortex: packed with immature T-cells
Inner medulla: where T-cells pass into as they mature
-both are laced w/ a network of epithelial cells, dendritic cells, & macphages, which interact physically with the developing thymocytes
Where are MHC antigens expressed & what are their gene products
Expressed at high density on the surface of cells of the thymic stroma
Class I: HLA-A, -B, -C
Class II: HLA-DP, -DQ, -DR
alpha chain plus beta-2 microglobulin, codominantly expressed, expressed on all nucleated cells of the body, CD8 cells
What Antigen Class?
MHC-Class I
Alpha and Beta chains, expressed codominantly, present on APC's, CD4 cells
What Antigen Class?
MHC-Class II
Positive Selection
TCRs capable of binding with low affinity; cells with "good" receptors
Failure of Positive Selection
those that fail to recognize self-MHC at all; cells with "useless" receptors
Negative Selection
those that bind to strongly to self MHC molecules will be induced to undergo apoptosis; cells with "bad" receptors
"helper" T cells (TH)
CD4+ cells that recognize class II MHC
Cytotoxic T cells (CTLs)
CD8+ cells that recognize class I MHC
What secondary lymphoid organ is designed to initate immune responses to tissue-borne antigens
Lymph nodes (small nodular aggregates found along lymphatic channels of body)
-filters tissue fluid
-Outer cortex Follicles = B-cell areas
-Paracortex = T-cell area
-Inner Medulla = Macrophages
What secondary lymphoid organ is designed to initate immune responses to blood-borne antigens
Spleen (filters blood)
What is the pathway of lymphatic circulation
Each LN is surrounded by a fibrous capsule punctured by an afferent lymphatic --> bring lymph into subcapsular sinus --> fluid percolates thru outter cortex (B-cell area) --> paracortex (T-cell area) --> inner medulla (macph) --> medullary sinus --> efferent lymphatic (memory cells exit) --> thoracic duct --> vena cava --> circulate
What is the pathway of circulation through the spleen
Splenic artery --> Arterioles surrounded by Periarteriolar lymphoid sheath, PALS (T-cell areas), Lymphoid follicles surrounded by rim of lymphocytes & macph attached nearby (B-cell areas) --> vascular sinusoids (Red pulp) --> splenic vein --> Portal circ
How to lymphocytes leave the bloodstream to enter lymph nodes?
High endothelial venules (HEVs)
-L-selectins on lymphocytes bind to addressins on the HEV, & chemokine receptors mediate the homing of specific cells to specific areas
-Naive T cells home to LN paracortex or splenic PALS
-Naive B cells migrate into LN follicles, & in spleen create a corona outisde the T-cell area
For a molelcule to be an immunogen/antigen, what 3 basic critera must it meet
-It must be recognized as foreign
-Must have a certain degree of chemical complexity
-Must have a molecular weight of at least 5,000 to 10,000 Kd
Portion of the Antigen that has 3-D complementarity with the idotype of a B-cell receptor or a TCR
Epitope/Antigenic Determinent of the Antigen
What is a Haptan
Single Antigenic Determinants
-they are to small to be recognized by the immune system to elicit an immune response
-however, they can become conjugated to body proteins (the carrier, i.e. RBCs) & the hapten-carrier conjugate serves as the immunogen for the ensuing allergic response
What is the first response to invasion
Acute Inflammatory Response, represents the response of the innate immune system
-First step is to activate the vascular endothemium in the breached epithelium barrier
-Cytokines & other inflam mediators are released to induce expression of selectin-type adhesion molecules
What is the first to bind to inflamed endothelium in acute inflammatory response
Neutrophils, they peak at about 6 hours
-Monocytes, macphs, & even eosinophils may arrive 5-6 hours later in response to neutrophil-released mediators
What are 4 sequential steps required for Extravasation of Phagocytes
(1) Rolling: Phagocytes (mucin-like adhesion mol) attach loosely to E-selectin on endothelium (force of bf in area causes cell to detach & reattach repeatedly --> rolling)
(2) Activatipn by Chemoattractants: Chemokines (i.e. IL-8, C5a, N-formyl peptides) bind R on phagocyte surface & trigger G-protein mediated activating signal --> induce confirmational change in integrins on phagocyte to inc affinity for Ig adhesion molecules on endothelium
(3) Arrest & Adhesion: Interaction b/w Integrins & Ig-CAMS mediates tight binding
(4) Transendothelial Migration: phagocyte extends pseudopodia thru vessel wall & extravasates into tissues & exhibit chemotaxis
Leukocyte Adhesion Deficiency
rare AR w/ absence of CD18 (common Beta-2 chain of integrin molecules)
-an inability of their leukocytes to undergo adhesion-dependent migration into sites of inflam
-1st Indication: Omphalitis (swelling & reddening around stalk of umbilical cord)
-suffer recurrent, chronic bacterial infections, have abnormally high # of granulocytes in their circ (cant migrate --> abscess & pus formation dont occur)
Method of Diagonising Leukocyte Adhesion Deficiency
Evaluating expression (or lack) of the beta chain (CD18) of the integrin by flow cytometry
Substances that are chemoattractive to neutrophils
IL-8, complement split product C5a, Leukotriene B4, Formyl methionyl peptides
Process of Phagocytosis involves
(1) Extension of pseudopodia to engulf attached material
(2) Fusion of pseudopodia to trap the material in a phagosome
(3) Fusion of phagosome w/ a lysosome to create a phagolysosome
(4) Digestion
(5) Exocytosis of digested contents
Opsonization is enhancement of phagocytosis with
How Staphylococcus aureus impede opsonization
Protein A of S. aureus impededs opsonization by binding to Fc component of IgG
What is respiratory burst
During phagocytosis, this metabolic process activates a membrane bound oxidase that generates oxygen metabolites which are toxic to ingested microorganisms
What reduces oxygen to superoxide anion, which generates hydroxyl radicals and hydrogen peroxide, which are microbicidal
NADPH oxidase
What is in the lysosome that acts on hydrogen peroxide & chloride ions to produce hypochlorite (active ingredient in household bleach), which is microbicidal
What are the lysosomal contents of phagocytes that contain oxygen-independent degradative materials
-Lysozyme (digests bacterial cell walls by cleaving peptidoglycan)
-Defensins (circular peptides that form channels in bacterial cell membranes)
-Lactogerrin (chelates iron)
-Hydrolytic enzymes
Intracellular Killing Mechanisms include:
Oxygen-Dependent Killing:
-Toxic Oxygen Metabolites (NADPH oxidase)
-Toxic Halide Radicals (Myeloperoxidase)
Oxygen-Independent Killing
-Lysosomal Contents
-->Hydrolytic enzymes
Inherited deficiency in the production of one of several subunits of NADPH oxidase that eliminates the phagocyte's ability to produce many critical O2-dependent intracellular metabolites
Chronic Granulomatous Disease: sufferent from chronic, recurrent infections w/ catalase (+) organisms (Staph, Klebsiella, Serratia, Aspergillus)

-Myeloperoxidase & Lysosomal content killing mech remain intact & they can fight over catalase (-) organisms
Nitroblue tetrazolium (NBT) reduction test or Neutrophil oxidative index can be used for what
Failures of phagocytic cells to generate oxygen radicals
--> used in Chronic Granulomatous Disease
4 bacteria that produce exotoxins that increase levels of cAMP (cAMP mnemonic)
c = cholera (Vibrio cholera)
A = anthrax (Bacillus anthracis)
M = Monteczuma's revenge (popular name for enterotoxigenic E. coli)
P = Pertussis (Bordetella pertussis)
How is the MHC I molecule loaded with peptides
Endogenous Pathway (i.e. Obligate IC pathogens, viral proteins)
-Proteins synthesized in cytosol are degraded in proteasomes into peptides
-Peptides are transported thru a peptide transporter, TAP complex into ER
-Bind to freshly syn MHC class I proteins
-Exocytosed & Transported to cell memb & presented to CD8+
How is the MHC II molecule loaded with peptides
Exogenous Pathway (i.e. EC
pathogens, Bacteria)
-Taken up into cell by APC's (small bacterial peptides w/in a vesicle)
-MHC II in ER are plugged w/ invarient chain, leave ER through exocytosis
-MHC II & nacterial vesicle fuse --> phagolysosome
-Dec acidity & component of phagolysosome cause invarient chain to degrade & opens up peptide binding groove
-Peptides in the vesicle are then loaded into the MHC II groove
-transported to cell surface of APC to be presented CD4+
What is the invarient chain
it is located on MHC class II molecules, blocks the peptide-binding groove so no normal cellular peptides can accidently be attracted there

-macph has both class I and class II binding sites since it is nucleated & an APC
What 3 signals are needed for T-cell activation
(1) Binding of TCR to MHC II/peptide commplex
(2) Costimulatory Molecules
-CD4 binds MHC II
-CD8 binds MHC I
-LFA-1 binds ICAM-1
-CD2 binds LFA-3
-CD28 binds B7
(3) Cytokines
-IL-2, IL-1, IL-6, TNF-alpha
How do CD4 & CD8 act as costimulatory molecules
the coreceptors for MHC classes II and I), tranduces activating signals to the T cells
How do Integrins on T-cells (LFA-1) & IgCAMs on APCs (ICAM-1) act as costimulatory molecules
they increase cell-cell adherence, so the cytokines can go back and forth

-also done by IgCAMs on T cells (CD2) binding to Integrins (LFA-3) on APCs
What triggers the upregulation of B7
Pathogen binding to innate receptors (e.g. TLR molecules) along w/ antigen recognition
What does CD28 on T cells binding to B7 on APC trigger
the transcription of several cytokines
What is the most important growth factor for T cells, that stimulates the proliferation of clones of T cells specific to that antigen
-the proliferation of naive T cells in response to antigen recognition is mediated by an autocrine growth pathway, the responding T cell secretes its own growth-promoting cytokine, IL-2, & also expresses the receptor molecules for it
What are the effector mechanisms controlled by Th cells
-Antibody synthesis (Th2)
-Macrophage Activation (Th1)
-Cytotoxic T-cell kills (Th1)
-NK cell killing
What cytokine causes macrophages to become activated
What are superantigens
Viral or bacterial proteins that cross-link the variable Beta domain of a TCR to an alpha chain of MHC II
-Cross-linkage provides an activating signal that induces T-cell activation & proliferation in absence of Ag-specific recognition of peptides in MHC II groove

Ex: Staphylococcal enterotoxins, Toxic-Shock Syndrome Toxin-1 (TSST-1), Streptococcal pyrogenic exotoxins
Where do superantigens bind on the TCR/MHC II complex and what are the consequences of this
They bind outside the Ag-binding cleft, they activate any clones of T cells expressing a particular variable Beta sequence & thus cause polyclonal activation of T cells resulting in overproduction of IFN-gamma
--> IFN-gamma activates macphs --> overexpression of proinflam cytokines (IL-1, IL-6, TNF-alapha) --> systemtic toxicity
What are the 2 major & 2 minor classes of Th cells that can arise from the naive T lymphocyte (Th0)
Th2: promote humoral immunity
Th1: promote CMI
Treg: regulate T cell activity
Th17: tissue damage assoc w/ autoimmune disease
What stimulates the differentiation of Th0 into Th1 cells
By microbes that stimulate a strong initial innate immune response w/ resultant production of IL-2, IFN-gamma, & TNF-beta

Caused by Intracellular Pathogens, Bacteria (i.e. Listeria, mycobacteria), & some parasites (i.e. Leishmania)
What stimulates the differentiation of Th0 into Th2 cells
Absence of innate immune stimuli, caused by Extracellular pathogens (i.e. Bacteria, helminths, response to allergens)
-promote humoral immunity, help make Abs, & help w/ class switching
-produced IL-4, IL-5, IL-6, IL-10, IL-13, TGF-beta
What is the role of IL-4, IL-5, and IL-10 in the Th2 response to Extracellular Pathogens
IL-4: Promotes class-switching to IgG & IgE, inhibits Th1 pathway to prevent differentiation to cause activated macphs
IL-5: promotes class-switching to IgA
IL-10: inhibits Th1 pathway to prevent differentiation to cause activated macphs
What is the role of IL-2 & IFN-gamma in the Th1 response to Intracellular Pathogens
IL-2: required for CTL to become cytotoxic
IFN-gamma: Activate macrophages & shuts down Ab response from Th2
What is the role of Treg cells produced from differentiation of Th0 cells
Regulate (inhibit) T cell fcn
-ID'd by constitutive expression of CD25 on surface & expression of TF FoxP3
-secrete inflammaiton inhibiting cytokines, IL-10, & are ciritical for the prevention of autoimmunity
What is the role of TH17 cells produced from differentiation of Th0 cells
believed to play a role in the tissue damage assoc w/ some autoimmune diseases
-ID'd by expression of TH RORgammat & production of pro-inflam cytokine IL-17
What type of leprosy has a strong Th1 response which is capable of eradicating the intracellular pathogens by granuloma formation
Tuberculoid Leprosy
-there is some damage to skin & peripheral nerves, but disease progresses slowly, if at all, & the pt survives
What type of leprosy has a strong Th2 response
Lepromatous Leprosy
-Th2 response is turned on, & because of reciprocal inhibition, the cell-mediated response is depressed
-pts develop Abs to the pathogen that are not protective & mycobacteria multiply inside macphs
-few macular lesions w/ multiple nodular lesions from bacterial overgrowth in tissues causing loss of sensation
-Hypergammaglobulinemia may occurs
What mediates humoral immunity
Antibodies syn by B lymphocytes & secreted by their fully differentiated end cell, the plasma cell
-directed toward the defense against EC microbes or toxins
What is needed for B-cell contact w/ Th cells (B lymphocyte activation)
-MHC II/peptide presentation
-Costimulatory Molecules (B7 is upregulated on the B lymphocytem making them effective presenters of Ag to Th cells in the area --> form a conjugate --> Th cell is activated & induced to a Th2 cell)
-CD40/CD40L binding (CD40L on surface of Th2 cell is upregulated & it interacts w/ CD40 on B cells)
What are the 3 signals needed for B cell activation
(1) MHC II/peptide presentation (Ag entering 2' lymphoid organs binds to & cross-links the idiotypes of these memb-R)
(2) CD40/CD40L binding (CD40L on surface of Th2 cell is upregulated & it interacts w/ CD40 on B cells)
(3) Release of Th2 cytokines
Th2 cytokines induce B-cell
-Differentiation into Ab secreting cells
-Memory cells
-Class Switching
Thymus Independent Antigens
-Contain no peptides (can't be recognized by T-cells)
--> i.e. Lipopolysaccharide from cell envelop of Gram (-) bacteria & polycapsular antigens
-Stimulate only IgM
-Create no memory
--> Response is generally weaker than the response to other classes of antigen
What are B-cell mitogens
Directly cause mitosis regardless of the cell's antigenic specificity
-Mitogens activate many clones of B cells & are used clinically to assess lymphocyte fcn
What is isotype switching
The progression of new antibody isotypes produced by B cells is defined by the sequence of constant domain coding in the B-lymphocute DNA & each isotype immunoglobulin is designed w/ a different effector fcn in mind (dictate effector fcn of Ab molecule)
-directed by Th2 cells
What occurs if an Ab molecule is digested with Papain
Cleavage occurs above the disulfide bonds that hold the heavy chains together
-generates 3 seperate fragments
--> 2 are called Fab (Fragment Antigen Binding), monovalent & capable of binding
--> 1 is Fc (Fragment Cystallizable)
What occurs if an Ab molecule is digested with Pepsin
Generates 1 large fragment called F(ab')2 & a digested Fc fragmet
--> F(ab')2 is divalent & is capable of binding & bridging
What is the bridging of Ags by Ab molecules required for
-Agglutinatinon of particulate antigens (RBCs and latex beads) or
-The precipitation of soluble antigens

--> IgG and F(ab')2 fragments both have a valence of 2 and can bridge b/w antigens
What is the first immunoglobulin that can be produced by a B cell w/ or w/o T-cell help & why
Coding for the constant domains of the heavy chain IgM (mu chains) are the 1st sequences downstream from the coding for the idiotype of the molecule
How does IgM exist on the surface of a B cell vs IgM secreted by plasma cells
Surface: Monomer
Secreted: Pentamer, help together in an extremely compact form by a J chain
Ig that has a plasma valence of 10, fcns in trapping of free antigen, and has the highest avidity of all Ig's
What Ig has the highest affinity

-interaction b/w the variable regions (Fab region) and the Antigen
What Ig is the most efficient at activating complement, is not an opsonin, and does not mediate ADCC
What is used as a measure of primary response (acute infection)
What will convalescent serum consist of
Mostly IgG's w/ subthreshold levels of IgM
What is needed for class-switching to take place
When and where does class-switching occur
Occurs during the immune response & occurs in the germinal centers (only formed during an immune response)
How is isotype-switching induced
B lymphocyte receives cytokine signals from the activated Th2 cells in the secondary lymphoid organs
What is isotype switching & how does it occur
It is the changing of the Hc constant domains to classes of Ab w/ new & different effector fcns
-by rearranging the DNA encoding the constant regions of Hc by activating switch regions that cause the intervening DNA to be looped out, excised, & degraded
-idiotype is then joined to a new constant region domain coding, & an Ab w/ identical Ag specificity but a new effector fcn is produced
What are the clones of proliferating antigen-specific B cells
Germinal centers in the follicles of the lymph nodes & spleen
What is it called when during intense proliferative response of the B cell, randome mutations in the coding of variable domain region may occur which can create a single point mutation in the Ab idiotype
Somatic Hypermutation
Clonal Selection
overtime clones of cells w/ high receptor affinity will begin to predominate in the germinal center and causes affinity maturation
Affinity Maturation
Predominance of clonses capable of producing Ab's w/ increasing affinity for the antigen
--> Although isotype switching will necessarily dec the avidity of the preponderance of Ab molecules as the immune response evolves, it will be substituded by an inc in Ab affinity over time
X-linked Hyper-IgM Syndrome
Characterized by deficiency of IgG, IgA, & IgE, and elevated levels of IgM
-Peripheral blood of infected pts has high #'s of IgM-secreting plasma cells, as well as autoantibodies to neutrophils, platelets, & RBCs
-they fail to make germinal centers during a humoral immune response
-defect is in gene encoding CD40L --> no CD40L expressed on Th cells --> o costimulatory signal for B-cell response to T-dependent Ags & only IgM is produced
Children with what condition suffer recurrent respiratory infections, esp those caused by Pneumocystis jiroveci
X-linked Hyper-IgM Syndrome
Major Ab produced after IgM, exists in 4 subisotypes, activates complement, opsonizes, & mediates ADCC, & actively transported across the placenta
Most is produced in the submucosa, dimer w/ a J chain, inhibits binding of adhesive substances to mucosal surfaces, important component of breast milk
What cytokines cause isotype switching to IgA
IL-5 & TGF-beta
What contains Th2 cells that assists in IgA production
MALT (mucosal-associated lymphoid tissues)
-the homing of specific memory cells to epithelial & mucosal surfaces leads to the production of these specialized lymphoid aggregations along these barriers
Where is MALT located
Tonsils, Peyer's patches, & numerous less well-organized lymphoid accumulations in the Lamina Propria
What receptor does IgA bind to so it is able to get into the submucosa
Poly Ig Receptor on the basolateral side of the epithelium
-it binds specifically to the J chain & transports the dimer across the cell & dumps it out into the mucosa
Secretory Component Function
When IgA is released into the mucosa, it steals the Poly Ig Receptor & that becomes the secretory component
-Transepithelial Transport
-Protection from proteolytic cleavage
What cytokines cause isotype switching to IgE
IL-4 and IL-13
Ig that is the so-called homocytotrophic Ab b/c it binds directly to FcSigma receptors present on mast cells & basophils (w/o binding Ag)
Mediates immediate type I allergic reactions & protects against parasites
What is the Ig that match the heavy chains
Mu: IgM
Gamma: IgG
Alpha: IgA
Delta: IgD
Sigma: IgE
Order of abundance of serum IgG
IgG (650-1,500) > IgA (75-390) > IgM (40-345) > IgD & IgE (trace)
Complement activation of classic pathway Ig
IgM, IgG
Opsonization Ig
Antibody-dependent cell-mediated cytotoxicity (ADCC)
Placental Transport Ig
Naive B-cell Antigen receptor
IgM, IgD
Memory B-cell antigen receptor (only one can be present)
IgG, IgA, IgE
Triggers mast cell granule release
In what type of deficiency do patients usually present w/ recurrent pyogenic infections w/ extracellular pathogens, absence of Ig's for opsonization & have a major problem w/ complement activation
Immunodeficiencies involving B Lymphocytes
-The T-cell Immune System is intact, & T-cell activies against IC pathogens, delayed-type hypersensitivity & tumor rejection are normal
Has two pathways of activation, enhances inflammation, enhances phagocytosis, & causes lysis
The Complement System
C3a, C4a, C5a
-C3a & C5a can bind directly to mast cells & basophils causing degranulation & release of Histamine
Main chemotactic complement protein
Main complement protein opsonin & Ab opsonin
C3b and IgG
What complement protein is responsible for clearance of immune complexes
How is the Alternative Complement Pathway initiated
By simple attraction of the early factors to the surface of microbes
-Bacterial polysaccharides & LPS of the cell envelope of Gram (-) bacteria
How is the Classical Complement Pathway initiated
Activated by Antigen-Antibody complexes
-Both IgG & IgM, but IgM is most efficient
Physiologic control on classical complement activation at the level of
C1, C3, & C5
Physiologic control on alternative complement activation at the level of
C3, C5
Deficiencies in membrane attack complex results in recurrent infections of
Uncontrolled complement activation at the mucosa surfaces cause edema & pain
Hereditary angioedema, deficiency of complement regulatory components
The absence of regulatory proteins causes paroxysms of hemolysis of RBCs and the resultant hemoglobinuria
Paroxysmal Nocturnal Hemoglobinuria, deficiency of complement regulatory components
What removed activated T cells after the Primary Immune Response
Activation-Induced Cell Death (AICD)
What type of B Lymphocytes have the highest affinity of Ig
Memory Lymphocytes: Highest affinity
Activated/Effector Lymphocytes: Increasing affinity
Naïve Lymphocytes: Low affinity
What type of T Lymphocytes have the highest amount of IL-2 Receptor Expressed
Activated/Effector Lymphocytes have the highest amount
Naïve & Memory Lymphocytes have the lowest amounts
Where do Memory Lymphocytes tend to home too
Home in a tissue-specific fashion, presumably returning to the type of tissue in which they first encountered Antigen
Where do Activated/Effector Lymphocytes tend to home too
Areas of active inflammation b/c of their expression of cell adhesion molecules such as LFA-1
Where do Naïve Lymphocytes tend to home too
Regions of secondary lymphoid organs specific for their cell type

Ex: T cells to paracortical areas
What mediates Activation-Induced Cell Death (AICD)
Mediated thru the Fas pathway
-Trimerization of the Fas molecule expressed on the surface of activated T cells w/ the Fas ligand molecule on neighboring cells initiates a signal-transduction cascade that leads to apoptosis of the Fas-bearing cell
As pathogens are eliminated by effector mechanisms & the system is slowly returning to its baseline quiescent state what is generated?
Immunologic memory, important b/c:
-avoids expending E on the generation of cells & molecules no longer needed & that may be potentially harmful in absence of invading stimulus
-“resets” the baseline homeostatic function of immunologic organs
How is B cell activity stopped after the Primary Immune Response
B lymphocyte differentiation into plasma cells is antigen-dependent, & as Ag disappears, the stimulus for differentiation is removed. Plasma cells only live 2 weeks & when they die they are not replaced from the differentiation B-cell pool, the response wanes
How do Memory B lymphocytes differ from Naïve B Lymphocytes
They have undergone isotype switching, & will have surface IgG, IgA, or IgE isotype & enter a resting stage of the cell cycle
What is the time lag after immunization & the peak response for a Primary Response vs a Secondary Response
Primary Response: 5-10 days, small peak
Secondary Response: 1-3 days, large peak
What is the passive means of Natural Immunity
Placental IgG transport, colostrum
What is the goal of passive immunization
Elicitation of protective immunity and immunologic memory
What is the goal of passive immunization
Transient protection or alleviation of existing condition
What is the immunization protocol for a Primary Response vs a Secondary Response
Primary Response: high dose of antigen (often w/ adjuvant)
Secondary Response: low dose of antigen (often w/o adjuvant)
What is the inducing agent for a Primary Response vs a Secondary Response
Primary Response: All immunogens
Secondary Response: Protein Antigens
What is the Antibody Isotype & Antibody Affinity for a Primary Response vs a Secondary Response
Primary Response: IgM, then IgG, variable to low antibody affinity
Secondary Response: Increasing IgG, IgA, or IgE, high Ab affinity (affinity maturation)
What is the morphology of Naïve Lymphocytes, Activated/Effector Lymphocytes, Memory Lymphocytes
Naïve Lymphocytes: Small, little cytoplasm
Activated/Effector Lymphocytes: Large, more cytoplasm
Memory Lymphocytes: Small
What is the active means of Natural Immunity
Recovery from infection
What is the passive means of Artificial Immunity
Horse antivenin against black widow spider bite, snake bite
Horse antitoxin against botulism, diphtheria
Pooled human immune globulin versus hepatitis A & B, measles, rabies, varicella zoster, or tetanus
“Humanized” monoclonal antibodies versus RSV
Recommended age for Diphtheria, Tetanus, Pertussis vaccine, DTaP
15-18 months, 4-6 years
Recommended age for Varicella vaccine, Varicella series
Varicella: 12-15 months, 4-6 years
Varicella Series: 7-18 years
Recommended age for Measles, Mumps, Rubella vaccine, MMR, MMR series
MMR: 12-15 months, 4-6 years
MMR series: 7-18 years
Recommended age for Influenza vaccine
6 months on, yearly
Recommended age for Inactivated polio vaccine, IPV, IPV series
IPV: 6-18 months, 4-6 years
IPV series: 7-18 years
Recommended age for Pneumococcal vaccine, PCV
12-15 months, 2-6 years at high-risk
Recommended age for Haemophilus influenza type B, Hib
12-15 months
What is the active means of Artificial Immunity
Hepatitis B component vaccine
Diphtheria, tetanus, pertussis toxoid vaccine
Haemophilus capsular vaccine
Polio live or inactivated vaccine
Measles, mumps, rubella attenuated vaccine
Varicella attenuated vaccine
Recommended age for Hepatitis B vaccine, HepB, HepB series
Hep B: 1-2 months, 6-18 months
HepB Series: 7-18 years
What are the risks associated with passive immunotherapy
From induction of antibodies from other species:
-IgE production (can cause systemic anaphylaxis)
-Type III Hypersensitivity (generate IgG or IgM anti-isotype Ab’s which form complement-activating immune complexes
From induction of antibodies from humans:
-Anti-allotype Antibodies (elicit response against minor Ig polymorphisms, allotypes)
What is the vaccine & vaccine type for B. pertussis
DTP, DTaP, Toxoid plus filamentous hemagglutinin
What viral vaccines can cause infections in immunocompromised host
Attenuated (Live): sometimes
Killed: no
Component: no
What viral vaccines can revert to a pathogenic form
Attenuated (Live): possibly
Killed: no
Component: no
What is the vaccine & vaccine type for N. meningitidis
MCV, 4 capsular serotypes (Y, W-135, C, A)
What is the vaccine & vaccine type for S. pneumoniae
Pediatric: PCV, 7 capsular serotypes & protein
Adult: PPV, 23 capsular serotypes
What is the vaccine & vaccine type for H. influenzae
Hib, Capsular polysaccharide and protein
What is the vaccine & vaccine type for C. tetani
DTP, toxoid
Recommended age for Hepatitis A vaccine, HepA & HepA series
HepA (2 doses) 12-23 months
HepA series 2-18 years
What is the vaccine & vaccine type for C. diphtheriae
DTP, toxoid
Recommended age for Meningococcal vaccine
2-18 years (high risk 2-10 years)
What viral vaccines have potential for contamination with other viruses
Attenuated (Live): yes, high
Killed: reduced
Component: no
Why are live attenuated viruses only given after 12 months of age?
Residual maternal antibodies would inhibit replication & the vaccine would fail
What vaccines are contraindicated in pt’s with egg allergies
Yellow Fever
What vaccines are contraindicated in pregnancy
Rubella (MMR)
What are the component vaccines of active immunization
Hepatitis B
What are the live viral vaccines of active immunization
Mrr. V.Z. Mapsy
-Varicella Zoster
-Adenovirus (pathogenic [not attenuated] respiratory strains given in enteric coated capsule
-Polio (Sabin)
-Small Pox
-Yellow Fever
(all by adenovirus is attenuated)
What are the killed viral vaccines of active immunization
RIP-A (Rest In Peace Always – the killed viral vaccines)
-Rabies (killed human diploid cell vaccine)
-Polio (Salk)
-A Hepatitis
What viral vaccines have immunogenicity
Attenuated (Live): High (CMI & HMI)
Killed: Lower (HMI)
Component: Middle
What viral vaccines have special storage
Attenuated (Live): yes, viable organisms
Killed: no
Component: no
In cases where children are at exceptionally high risk exposure to a pathogen, they are sometimes given earlier than 6-9 months of age, what is most often needed in these cases
The need for repeated booster inoculations
What is colostrum so important
Infant only has 20% of adult IgA at 12 months
What is the only isotype useful in diagonising infections in an neonate
Why do normal infants have few infections during the 1st few months
Maternal IgG
When do children w/ immune deficiencies become ill
When maternal IgG is low
What do vaccines need to elicit in order for an immune response to display immunogenic memory
Th cells
-live viral vaccines elicit CMI & HMI
-killed viral vaccine elicit antibodies
What type of vaccine is generally required for enveloped viruses
Live vaccines

-Killed vaccines are generally sufficient for naked viruses
What two vaccines are examples of Recombinant antigen vaccines
Hepatitis B & HPV
-Hep B: the gene coding for HBsAg is inserted into yeast cells, which then release this molecule into the culture medium, the molecule is then purified & used as the immunogen in the vaccine
What substances increase the immunogenicity of an antigen when administered with it
What effects can adjuvants exert
Prolonging antigen persistance (Aluminum potassium sulfate)
Enhancing costimulatory signals (muramyl dipeptide)
Inducing granuloma formation
Inducing nonspecific lymphocyte proliferation (LPS & synthetic polyribonucleotides)
What is an allotype
Minor amino-acid sequence variations in rgw constant domains of Hc and Lc Ig's
There expression is genetically determined, & repeated exposure to a foreign allotype can cause production of antibodies which recognize these sequence variations
Th1 cells primed in the lymph nodes and spleen serve to provide the cytokine stimuli to activate 3 potential effector cells to destroy infected or altered cells
NK cells
What arm of the immune response is designed to identify and eradicate antigenic stimuli that arise from inside the cells of the body
Cell-mediated Immune response
Kill intracellularly, killing is enhanced by IFN-gamma, TNF-alpha, and TNF-beta, cause granulomas & necrosis of surrounding tissues
When Th1 cells activate macrophages and cause tissue damage, the result is
Delayed-type hypersensitivity (DTH)
What assay is often used to measure the pts ability to mount a CMI response
DTH skin testing, i.e. Mantoux test, Lepromin Test
What does CTL stimulation require
-Non-self peptide/class I MHC
-IL-2 (secreted by Th1 cell to enhance differentiation & cloning)
-IFNs increase MHC expression (make targets more susceptible to killing)
What is the process by which CTLs kill their target in the Degranulation pathway
(1) Attachment to the target (mediated by TCR, CD8, LFA-1 integrin)
(2) Activation (cytoskeletal rearrangment to concentrate granules against attached targets)
(3) Exocytosis of granule contents (perforin & granzymes)
(4) Detachment from the targets
CTLs kill by
-Cytokines (TNF)
What are two mechanisms by which CTL killing can occur
(1) Degranulation with perforin & granzymes
(2) TNF/TNF receptor interaction (FasL on CTL binding to Fas on target cells)
kill tumor cells & virus infected cells, kill by granzymes and perforin, enhanced by IFN-alpha, IFN-beta, and IL-12, inhibited by MHC class I, counted with CD16 & CD56
NK cells
NK cell markers
CD16 and CD56
NK cells (#1), macrophages, monocytes, neutrophils, eosinophils, target recognition via IgG, killing by lytic enzymes, TNF, perforin
Antibody-Dependent Cell-mediated Cytotoxicity (ADCC)
What are the 2 mechanisms NK cells kill in CMI
(1) cells that do not have class I MHC
(2) Target recognition via IgG (ADCC)
What is the special case where IgE (not IgG) can mediate ADCC
When the target is a parasitic worm
Effector cells in CMI CD markers
NK cell
NK cell: CD16, CD56, CD2
Macrohphage: CD14
Effector cells in CMI, Antigen Recognition
NK cell
CTL: Specific, TCR
NK cell: ADCC (specific for IgG), otherwise recognizes lectins
Macrohphage: nonspecific
Effector cells in CMI, MHC recognition required for killing
NK cell
CTL: Yes, class I MHC
NK cell: No, MHC I recognition inhibits
Macrohphage: No
Effector cells in CMI, effector molecoles
NK cell
CTL: Perforin, Granzymes, Cytokines (TNF-beta, IFN-gamma)
NK cell: Perforin, Granzymes, Cytokines (TNF-beta, IFN-gamma)
Macrohphage:TNF-alpha (IL-1, IL-6), Enzymes (NADPH oxidase, myeloperoxidase), NO, oxygen radicals
What virus downregulates class I MHC & also produces a "decoy" MHC class I molecule
Deficiency in NADPH oxidase, failure to generate superoxide anion & other O2 radicals, recurrent infection w/ catalase-positive bacteria & fungi
Chronic Granulomatous Disease (CGD)
Absence of CD18, recurrent & chronic infections, failure to form pus, & do not reject umbilical cord stump, often have a lot of gingivostomatitic
Leukocyte adhesion deficiency
Granule structural defect, recurrent infection w/ bacteria, chemotactic & degranulation defects; absent NK activity, partial albinism
Chediak-Higashi syndrome
Pt w/ albinism & an immune deficiency
Chediak-Higashi syndrome
Deficiency of essential enzyme in hexose monophosphate shunt, same Sx as CDG with assoc anemia
Glucose-6-phosphate dehydrogenase (G6PD) deficiency
Granule enzyme deficency with mild or no Sx, cell is unable to generate hypochlorite
Myeloperoxidase defiency
Th1 cells can't make IFN-gamma, neutrophils dont respond to chemotactic stimuli, coarse facies, cold abscesses, retained primary teeth, increased IGE, eczema
Job's Syndrome
Deficiency of BTK, blocks B-cell maturation, low Ig's of all classes, no circulating B cells, B-cell maturation in bone marrow stopped at pre-B stage, normal CMI; Tx w/ monthly gamma globulin replacments, ABX for infection
Bruton X-linked Hypogammaglobulinemia
Deficiency of CD40L on activated T cells, high serum titers of IgM w/o other isotypes, normal B & T-cell numbers, susceptibility to EC bacteria & oppurtunists, Tx w/ ABX & gammaglobulins
X-linked Hyper-IgM syndrome
Deficiency of IgA, repeated sinopulmonary & GI infections, Tx w/ ABX not Ig's
Selective IgA deficiency (most common)
Molecular defect is unknown, onset in late teens to early 20's, B cells present in peripheral blood, Ig levels dec w/ time, inc autoimmunity, inc atopy, Tx w/ ABX
Common Variable Immunodeficiency
Delayed onset of normal IgG syn, detected in 5th to 6th month of life; resolves by 16-30 months; susceptibility to pyogenic bacteria; Tx w/ ABX & in severe cases gammaglobulin replacement
Transient Hypogammaglobulinemia of Infance
What is the normal immunologic event that does not occur in pts w/ X-linked Hyper-IgM syndrome
Isotype Class switching
Deficiency in Classic Pathway, marked inc in immune complex diseases, increased infections w/ pyogenic bacteria
Deficiency in C1q, C1r, C1s, C4, C2,
Deficiency in both complement pathways, very severe recurrent bacterial infections & immune complex disease
Deficiency in C3,
Defiency in both complement pathways, recurrent meningococcal & gonococcal infections
Deficiency in C5, C6, C7, or C8
Deficiency in complement regulatory proteins, overuse of C1, C4, or C2, with edema at mucosal surfaces
Deficency in C1- inhibitor --> Hereditary Angioedema
What are the Selective T-cell deficiencies
DiGeorge Syndrome
MHC class I Deficiency
Bare Lymphocyte Syndrome (MHC class II Deficiency)
Failure of formation of 3rd & 4th pharyngeal pouches, thymic aplasia, Facial abnormalities, hypoPT, cardiac malformations, depression of T-cell #'s & absence of T-cell responses
DiGeorge Syndrome
Failure of TAP 1 molecules to transport peptides to ER, CD8+ T cells deficient, CD4+ T cells normal, recurrent viral infections, normal DTH, normal Ab production
MHC class I Deficiency
Failure of MHC class II expression, defects in transcription factors, T cells present & responsive to nonspecific mitogens, no GVDD, deficient in CD4+ T cells, hypogammaglobulinemia
Bare Lymphocyte Syndrome (MHC class II Deficiency)
What is the only Ab Isotype present in DiGeorge Syndrome
-T-cells are needed for IgG, IgA, and IgE Ab production
What are the combined partial B- and T-cell deficiencies
Wiskott-Aldrich Sydrome
Defect in cytoskeletal glycoprotein, X-linked, defective responses to bacterial polysaccharides & depressed IgM, gradual loss of humoral & cellular responses, thrombocytopenia, & eczema
Wiskott-Aldrich Sydrome
Defect in kinase involved in cell cycle, ataxia, telangiectasia (capillary distortions in eye), Deficiency of IgA & IgE production
Present with Triad of Sx: Immunodeficiency, Eczema, Thrombocytopenia
Wiskott-Aldrich Sydrome
What is the complete functional B- and T-cell deficiency and what are the subtypes
Severe Combined Immunodeficiency (SCID)
-Defects in common gamma chain IL-2 receptor (present in IL-4,IL-7, IL-9, IL-15), X-linked
-Adenosine Deaminase Deficiency (results in toxic metabolic products in cells)
-rag1 or rag2 gene nonsense mutations
What Severe Combined Immunodeficiency (SCID) subtype has total absence of B and T cells
rag1 or rag2 gene nonsense mutations
Severe Combined Immunodeficiency (SCID) subtype that present with chronic diarrhea; skin, mouth, and throat lesions; opportunisitc (fungal) infections; low levels of circulating lymphocytes; cells unresponsive to mitogens
-Defects in common gamma chain IL-2 receptor (present in IL-4,IL-7, IL-9, IL-15), X-linked
-Adenosine Deaminase Deficiency
Early in HIV infection where does the virus bind
-D-type retrovirus attaches to CD4 receptors on host cells (Th cells, macphs, microglial)
-CCR5 chemokine receptor on the macrophage
Late in HIV infection where does the virus bind
CXCR4 chemokine receptor on the T-cells
What gene is responsible for HIV virulence by making infected cells less susceptible to CTL killing
Nef gene product, downregulates class I MHC expression
What HIV characteristic is responsible for eliminating cell- and antibody-mediated immunity
Direct cytopathic effect on lymphocytes & macrophages
What HIV characterisitic inhibits cytokine syn in both infected & uninfected cells
Tat gene product
What does Immune deviation toward the Th2 in HIV cause?
Inhibits potentially protective CMI responses and produces Abs that can mediate ADCC, resulting in further elimination of TH cells
What results from the antigenic drift of gp120
Evades antibody mediated effector mechanisms and exhausts individuals immune capacity
What results from the heavy glycosylation of gp120
Hides potentially protective epitopes from immune recognition
What is the reservoir for HIV infection
If you have pt that has known sexual encounters w/ HIV (+) individuals, uses no protection or prophylaxis and has never been HIV (+), what molecule is responsible for this
CCR5 mutation
-Homozygous = immune
-Heterozygous = slows clinical course
What is caused by excessive responses to foreign antigens, or failure of self-tolerance (autoimmunity)
Hypersensitivity disease
What do all hypsensitivity reactions have in common
-The first exposure to the antigen "sensitizes" the lymphocyes
-Subsequent exposures elicit a damaging rxn
-The response is specific to a particular antigen or a cross-reacting substance
IgE mediated, protective response to helminth, atopic/allergic individuals develop this response to inappropriate stimuli
Type I (immediate) Hypersensitivities
Primary mediators of Type I hypersensitivity
Mediators that are already made & stored in the granule
-Eosinophil chemotactic Factor A (multiple chemokines)
Histamine of Type I hypersensitivity
Smooth muscle contraction; inc vasc permeability
Heparin of Type I hypersensitivity
Eosinophil chemotactic Factor A of Type I hypersensitivity
Secondary mediators of Type I hypersensitivity
Newly synthesized from Arachidonic Acid
-Prostaglandin D2, E2, F2alpha
-Leukotrienes C4, D4, E4 (lipoxygenase pathway)
-Leukotriene B4
Prostaglandin D2, E2, F2alpha
of Type I hypersensitivity
Inc Smooth muscle contraction & vasc permeability
Leukotrienes C4, D4, E4 of Type I hypersensitivity
Inc Smooth muscle contraction & vasc permeability
Leukotriene B4 of Type I hypersensitivity
Chemotactic for neutrophils
What is responsible for the late-phase rxn of Type I hypersensitivity
Arachidonic Acid cascade --> breakdown of phospholipids in membrane that get shuttled through this pathway
Allergens: Trees, grasses, dust, cats, dogs, mites
Clinical Findings: Edema, Irritation, mucus in nasal mucosa
Allergic rhinitis (Hay Fever), Type I hypersensitivity
Allergens: Insect stings, drug reactions
Clinical Findings: Bronchial & tracheal constriction, complete vasodilation & death
Systemic Anaphylaxis, Type I hypersensitivity
Allergens: Milk, eggs, fish, cereals, grains
Clinical Findings: Hives & GI problems
Food allergies, Type I hypersensitivity
Allergens: In vivo skin testing for allergies, insect bites
Clinical Findings: local skin edema, reddening, vasodilation of vessels
Wheal & Flare, Type I hypersensitivity
Allergens: Inhaled materials
Clinical Findings: Bronchial & tracheal constriction, edema, mucus production, massive inflammation
Asthma, Type I hypersensitivity
What is the development of Immediate-Hypersensitivity Reaction
(1) First exposure to allergen
(2) Th2 release of IL-4 & IL-13 stimulates B cells to produce IgE; class switching occurs
(3) B cell produces IgE immunoglobulin; it attaches to Fc receptor on mast cell
(4) Second Exposure to allergen
(5) Allergen cross-links several IgE molecules on mast cell & cell degranulates releasing powerful chemicals
Type I Effector Cells
Mast Cells
Activated Mast Cell (or basophil) effects:
Biogenic amines (histamine)
Lipid Mediators (PAF, PGD2, LTC4)
Cytokines (TNF)
Enzymes (trypase)
Biogenic amines (histamine): Vascular leakage, bronchoconstriction
Lipid Mediators (PAF, PGD2, LTC4): Bronchoconstriction, intestinal hypermotility, inflammation, tissue damage
Cytokines (TNF): Inflammation
Enzymes (trypase): Tissue damage
Eosinophil Effects:
Cationic granule proteins (major basic protein, eosinophil cationic protein)
Enzymes (eosinophil peroxidase)
Cationic granule proteins (major basic protein, eosinophil cationic protein): kill of parasites & host cells
Enzymes (eosinophil peroxidase): tissue remodeling, kill of parasites & host cells
How antibodies in Type II Hypsensitivities cause tissue damage
(1) May opsonize or activate the copmlement system
(2) May recruit neutrophils and macrophages that cause tissue damage
(3) May bind to normal cellular receptors and interfere with their fcn
Tissue-specificc autoantibodies, opsonize or activate copmlement, recruit inflammatory cells, interfere with cellular fcn
Type II Hypsensitivities
What are the types of Cytotoxic Type II Hypsensitivities
Autoimmune Hemolytic Anemia (HDNB)
Acute Rheumatic Fever
Goodpasture System
Transfusion Reaction
Autoimmune Thrombocytopenic purpura
Ab to RBC membrane proteins (Rh, I, Ags) --> Opsonization, phagocytosis, & complement-mediated destruction of RBCs --> Hemolytic anemia
Autoimmune Hemolytic Anemia (HDNB), Cytotoxic Type II Hypsensitivity
Ab against stretococcal cell-well Ag; Ab cross-reacts w/ myocardial Ag --> inflammation, macrophage activation --> myocarditis arthritis
Acute Rheumatic Fever, Cytotoxic Type II Hypsensitivity
Ab against type IV collage in basement membrane of kidney glomeruli & lung alveoli --> complement- & Fc-receptor mediated inflammation --> Nephritis, lung hemorrhage, linear Ab depositons on IF
Goodpasture System, Cytotoxic Type II Hypsensitivity
Ab against ABO blood glycoproteins --> IgM isohemagglutinins formed naturally in response to normal bacterial flora cause opsonization + complement activation --> hemolysis
Transfusion Reaction, Cytotoxic Type II Hypsensitivity
Ab against platelet membrane proteins --> Ab-mediated platelet destruction through opsonization & complement activation --> bleeding
Autoimmune Thrombocytopenic purpura, Cytotoxic Type II Hypsensitivity
What are the types of Non-cytotoxic Type II Hypsensitivities
Myasthenia Gravis
Graves disease
Type II (non-insulin dependent diabetes)
Pernicious Anemia
Ab against ACh receptor --> Ab inhibits ACh binds, downmodulates receptors --> Muscle weakness, paralysis
Myasthenia Gravis, Non-cytotoxic Type II Hypsensitivity
Ab against TSH receptor --> Ab-mediated stimulation of TSH receptors --> Hyperthyroidism followed by Hypothyroidism
Graves disease, Non-cytotoxic Type II Hypsensitivity
Ab against Insulin receptor --> Ab inhibits binding of insulin --> Hyperglycemia
Type II (non-insulin dependent diabetes), Non-cytotoxic Type II Hypsensitivity
Ab against instrinsic factor of gastric parietal cells --> Neutralization of intrinsic factor, decreased absorption of Vit B12 --> abnormal erythropoiesis, anemia
Pernicious Anemia, Non-cytotoxic Type II Hypsensitivity
How is Type II Hypsensitivity different from Type III Hypsensitivity
In Type II Hypsensitivity as the disease progresses, complexes of Antigen & antibody may cause localized damage, but these complexes do not circulate so the damage is localized to the specific tissue
Anti-RhD + IgG, formed in Rh- mother carrying an Rh+ child, first preganancy sensitizes, Ab crosses placenta and injures subsequent fetuses, prevent w/ RhoGAM
Hemolytic disease of the Newborn (HDNB) a.k.a. Erythroblastosis fetalis, Type II Hypsensitivity
What is RhoGAM and when is it used
A preparation of human Anti-RhD IgG antibody, used to prevent hemolytic disease of the newborn in an Rh- mother
-it is given at 28 weeks gestation & again w/in 72 hours after birth
-this Ab effectively eliminates the fetal Rh+ cells before they can generate RhD-specific memory B cells in the mother
Systemic damage, Immune complexes activate complement, self or foreign Antigens
Type III Hypsensitivity
What are examples of Type III Hypsensitivities
Systemic Lupus Erythematosus
Rheumatoid Arthritis
Poststreptococcal Glomerulonephritis
Serum Sickness
Arthus Reaction
Abs against dsDNA, Sm, & other nucleoproteins --> nephritis, arthritis, vasculitis, butterfly facial rash
Systemic Lupus Erythematosus, Type III Hypsensitivity
Target antigen is Rheumatoid Factor --> joint pain, erosions
Rheumatoid Arthritis, Type III Hypsensitivity
Target antigen is streptococcal cell wall Ags (may be "planted" in GBM) --> Nephritis, "lumpy-bumpy deposits"
Poststreptococcal Glomerulonephritis, Type III Hypsensitivity
Caused by various proteins (i.e. giving immunoglobulins or anti-venom) --> Arthritis, vasculitis, nephritis
Serum Sickness, Type III Hypsensitivity
Caused by any injection protein --> Localized pain & edema
Arthus Reaction, Type III Hypsensitivity
What is Rheumatoid Factor
Your own IgM against your own IgG that is specific to the Fc portion
Delayed-type (48-72 hours), CD4+ Th1 cells mediate, activate macrophages, cause inflammation, common in chronic intracellular infections
Type IV Hypsensitivity
What are examples of Type IV Hypsensitivities
Tuberculin test (PPD)
Contact Dermatitis
Hashimoto's thyroiditis
Insulin-dependent diabetes mellitus (Type I)
Multiple Sclerosis
Guillain-Barre Syndrome
Celiac Disease
PPD (tuberculin & mycolic acid) --> Indurated skin lesion (granuloma)
Tuberculin test (PPD), Type IV Hypsensitivity
Nickel, poison ivy/oak, catechols, hapten/carrier --> vesicular skin lesions, pruritis, rash
Contact Dermatitis, Type IV Hypsensitivity
Unknown Ag in thyroid --> Hypothyroidism
Hashimoto's thyroiditis, Type IV Hypsensitivity
Islet-cell antigens, insulin, glutamic acid decarboxylase, etc --> Polydipsia, Polyuria, Polyphagia, Ketoacidosis
Insulin-dependent diabetes mellitus (Type I), Type IV Hypsensitivity
Target antigen is streptococcal cell wall Ags (may be "planted" in GBM) --> Nephritis, "lumpy-bumpy deposits"
Poststreptococcal Glomerulonephritis, Type III Hypsensitivity
Caused by various proteins (i.e. giving immunoglobulins or anti-venom) --> Arthritis, vasculitis, nephritis
Serum Sickness, Type III Hypsensitivity
Caused by any injection protein --> Localized pain & edema
Arthus Reaction, Type III Hypsensitivity
What is Rheumatoid Factor
Your own IgM against your own IgG that is specific to the Fc portion
Delayed-type (48-72 hours), CD4+ Th1 cells mediate, activate macrophages, cause inflammation, common in chronic intracellular infections
Type IV Hypsensitivity
What are examples of Type IV Hypsensitivities
Tuberculin test (PPD)
Contact Dermatitis
Hashimoto's thyroiditis
Insulin-dependent diabetes mellitus (Type I)
Multiple Sclerosis
Guillain-Barre Syndrome
Celiac Disease
PPD (tuberculin & mycolic acid) --> Indurated skin lesion (granuloma)
Tuberculin test (PPD), Type IV Hypsensitivity
Nickel, poison ivy/oak, catechols, hapten/carrier --> vesicular skin lesions, pruritis, rash
Contact Dermatitis, Type IV Hypsensitivity
Unknown Ag in thyroid --> Hypothyroidism
Hashimoto's thyroiditis, Type IV Hypsensitivity
Islet-cell antigens, insulin, glutamic acid decarboxylase, etc --> Polydipsia, Polyuria, Polyphagia, Ketoacidosis
Insulin-dependent diabetes mellitus (Type I), Type IV Hypsensitivity
Myelin basic protein, proteolipid protein --> progressive demyelination, blurred vision paralysis
Multiple Sclerosis, Type IV Hypersensitivity
Peripheral nerve myelin or ganglioside --> ascending paralysis, peripheral nerve demyelination
Guillan-Barre Syndrome, Type IV Hypersensitivity
Unknown specificity of pathogenic T cells --> Gluten sensitive enteropathy
Celiac Disease, Type IV Hypersensitivity
What is the Ab, complement, and Effector cells of Type I (immediate) Hypersensitivity rxns
Ab: IgE
Complement: No
Effector Cells: Basophil, mast cell

Ex: Hay fever, atopic dermatitis, insect venom sensitivity, anaphylaxis to drugs, some food allergies, allergies to animals & animal products, asthma
What is the Ab, complement, and Effector cells of Type II (cytotoxic) Hypersensitivity rxns
Ab: IgG, IgM
Complement: Yes
Effector Cells: PMN, macrophages, NK cells

Ex: Autoimmune or drug-induced hemolytic anemia, transfusion rxns, HDNB, hyperacture graft rejection, Goodpasture's disease, Rheumatic Fever
What is the Ab, complement, and Effector cells of Type II (non-cytotoxic) Hypersensitivity rxns
Ab: IgG
Complement: No
Effector Cells: None

Ex: Myasthenia gravis, Graves disease, Type 2 DM
What is the Ab, complement, and Effector cells of Type III (Immune Complex) Hypersensitivity rxns
Ab: IgG, IgM
Complement: Yes
Effector Cells: PMN, macrophages

Ex: SLE, RA, polyarteritis nodosa, poststreptococcal GN, Arthus rxn, Serum sickness
What is the Ab, complement, and Effector cells of Type IV (Delayed, DTH) Hypersensitivity rxns
Ab: None
Complement: No
Effector Cells: CTL, Th1, Macrophages

Ex: Tuberculin test, TB, Leprosy, Hashimoto thyroiditis, poison ivy (contact dermatitis), acute graft rejection, GVHD, IDDM
How do you differentiate b/w Multiple Sclerosis and Myasthenia Gravis
MS: Spastic paralysis
MG: weakening paralysis
What is a common infection causing Guillain-Barre Syndrome
Failure of self-tolerance, Genetics (class II MHC), Environment (infections), Hormones
What is the key factor in the development of autoimmunity
the recognition of self-antigens by autoreactive lymphocytes, which then become activated, proliferate, and differentiate to produce effector cells and cytokines that cause tissue injury
What is among the strongest genetic associations w/ development of autoimmune disease?
class II MHC genes
HLA allele in Rheumatoid Arthritis
HLA allele in Insulin-dependent DM (Type I)
HLA allele in Multiple Sclerosis, Goodpasture's
HLA allele in SLE, Psoriasis, IBD, Reiter's syndrome
HLA allele in Ankylosing Spondylitis
HLA allele in Celiac Disease
DQ2 or DQ8
HLA allele in Graves disease
Immune responses may recruit leukocytes and increase of expression of costimulators which activate T lymphocytes that are not specific for the infectious pathogen
Bystander activation
Antigens of a microbe cross-react w/ or mimic self antigens
Molecular Mimicry
Can expose self antigens that are normally concealed from immune cells
Inflammation and associated damage
Infections can trigger autoimmunity through
-activating bystanders
-molecular mimicry
-inflammatory damage
What is the mainstain of therapy for hypersensitivity disease directed at
Modification of T-cell function
-inhibit T cell proliferation
-inhibit T cell function
-kills T cells
-antagonize damaging products
What therapy for immune diseases inhibits T cell proliferation
What therapy for immune diseases inhibit T cell function
What therapy for immune diseases kills T cells
What therapy for immune diseases are antagonists to proinflammatory cytokines or costimulatory molecules
Monoclonals or binding proteins
How are monoclonal antibodies produced?
By fusing antigen-specific spleen cells with myeloma cells --> this causes the production of identical, monospecific Abs b/c they are all produced by a single, cloned, parent cell
Clinical use of Abciximab
Antiplatelet: Antagonist of IIb/IIIa receptors
Clinical use of Infliximab
RA & Crohn's disease: binds TNF
Clinical use of Trastuzumab
Breast CA: antagonists to ERB-B2
Clinical use of Dacliximab
Kidney Transplants: Blocks IL-2 receptors
Clinical use of Muromonab
Kidney Transplant: blocks allograft rejection, blocks CD3
Clinical use of Palivizumab
Respiratory syncytial virus: blocks RSV fusion protein
Clinical use of Rituximab
Non-Hodgkin Lymphoma: binds CD20
When tissue is moved from one location to another in the same individual
Autografts (Autologous grafts)

Ex: Skin grafting in burns or Coronary Artery Replacement with Saphronous veins
Skin grafting in burns or Coronary Artery Replacement with Saphronous veins
Transplants b/w genetically identical individuals (monozygotic twins)
Isografts (Syngeneic grafts)
Grafts transplants b/w genetically different members of the same species
Allogeneic grafts

Ex: Kidney Transplant
Kidney Transplant
Allogeneic grafts
Grafts transplanted b/w members of a different species
Xenogeneic grafts

Ex: Baboon heart into human child
Baboon heart into human child
Xenogeneic grafts
All grafts except what are identified as foreign invading proteins and destroyed by Graft rejection
Graft Rejection Effectors
Effector Phase of Rejection
Th cytokines play a critical role in stim macph, Cytotoxic T cell, & Ab-mediated killing
-IFNs, TNF-alpha & -beta all inc the expression of class I MHC
-IFN-gamma inc the expression of class II MHC, as well as increasing the susceptibility of cells in the graft to MHC-restricted killing
Types of Graft Rejection
Caused by a bone marrow transplants where grafted T cells attack the host, Sx include Rash, jaundice, diarrhea, GI hemorrhage
Graft-verus-Host-Disease (GVHD)
Tissue Compatibility testins
ABO Blood typing
Mixed Lymphocyte reaction (class II)
Microtoxicity test (class I)
Routine HLA Typing
-these are the only loci that appear to predict the likelihood of rejection of the transplantq
Microtoxicity test (class I)
Using antisera against specific class I antigens
-Lymphocytes from the donor or recipient are mixed w/ different antisera
-If Abs recognize their specific epitope on the cells they will be bound there & addition of complement will result in cell lysis
-the lysis of cells is monitored by adding a dye that will penetrate cells whose memb have become leaky from the actions of complement
Mixed Lymphocyte reaction (class II)
-Lymphocytes from one individual being tested are irradiated so that they cannot proliferate but will act as stimulator cells for the presentation of MHC antigens
-the other individual's cells are added to the culture & uptake of tritrated thymidine is used as an indicator cell proliferation
-if the MHC class II antigens are different, proliferation will occur, if they are the same, no proliferation will occur
Cyclosporin A
Prevention of acute allograft rejection
-drug inhibits IL-2 & also IL-2 receptors, thereby effectively preventing lymphocyte proliferation
Some Killers Have Pretty Nice Capsules
Streptococcus pneumoniae
Klebsiella pneumoniae
Haemophilus influenza
Pseudomonas aeruginosa
Neisseria meningitidis
Cryptococcus neoformans
Primary mechanism of adherence in most gram (-) cells
Primary mechanism of adherence in gram (+) cells
Teichoic acids
Cleaves Fc portion may coat bacteria & bind them to cellulara Fc receptors
IgA proteases
Destruction of mucosa IgA

Ex: Neisseria, Haemophilus, S. pneumoniae
Chelate and import iron
Surface proteins that allow an organism to bind and invade normally non-phagocytic human cells, escaping the immune system

Ex: Yersinia pseudotuberculosis (organism causing diarrhea)
Tunnel from the bacteria to the host cell (macrophage) that delivers bacterial toxins directly to the host cell
Type III Secretion Systems

Ex:E. coli, Salmonella species, Yersinia species, P. aeruginosa, Chlamydia
What is the toxic portion of LPS
Lipid A
What toxins are the inhibitors of protein synthesis
Corynebacterium diptheriae (Diphtheria toxin)
Pseudomonas aeruginosa (Exotoxin A)
Shigella dysenteriae (Shiga toxin)
Enterohemorrhagic E. coli (Verotoxin, a shiga-like toxin)
Mode of action of Diphtheria toxin
ADP ribosyl transferase; inactivates eEF-2; 1' targets: heart/nerves/ epithelium
--> inhibits eukaryotic cell protein cell synthesis
Mode of action of Exotoxin A (pseudomonas aeruginosa)
ADP ribosyl transferase; inactivates eEF-2; 1' target: liver
--> inhibits eukaryotic cell protein cell synthesis
Mode of action of Shiga Toxin (Shigella dysenteriae)
Interferes w/ 60S ribosomal subsunit
inhibits protein cell synthesis in eukaryotic cells
Mode of action of Verotoxin (EHCH)
Interferes w/ 60S ribosomal subsunit
inhibits protein cell synthesis in eukaryotic cells
What are the neurotoxins
Clostridium tetani (Tetanus Toxin)
Clostridium botulinum (Botulinum Toxin)
Mode of action of Tetanus Toxin
Blocks release of the inhibitory neurotransmitters glycine & GABA
-inhibits protein syn in euk cells
Mode of action of Botulinum Toxin
Blocks release of ACh
-inhibitos cholinergic synapse
What are the superantigens
Staphylococcus aureus (TSST-1)
Streptococcus pyogenes (Exotoxin A a.k.a. erythrogenic or pyrogenic toxin)
What are the cAMP inducers
Enterotoxigenic E. coli (Heat labile toxin (LT))
Vibrio cholerae (Cholera toxin)
Bacillus anthracis (Anthrax toxin)
Bordetella pertussis (Pertussis Toxin)
Mode of Action of Heat Labile Toxin (LT, ETEC)
LT stim an adenylate cyclase by ADP ribosylation of GTP binding protein
Mode of Action of Anthrax Toxin
EF = edema factor = adenylate cyclase
LF = lethal factor
PA = protective antigen
Mode of Action of Pertussis Toxin
APD ribosylates Gi, the negative regulator of adenylate cyclase --> inc cAMP
-Histamine-sensitizing Lymphocytosis promoting Islet activating
What are the cytolysins
Clostridium perfringens (Alpha toxin)
Staphylcoccus aureus (Alpha toxin)
What is Mode of Action of Alpha toxin in Clostridium perfringens
-damages cell membranes; myonecrosis
What is Mode of Action of Alpha toxin in Staphylcoccus aureus
Toxin intercalates forming pores
-cell memb becomes leaky
Outer membrane
Gram (-) only
Hydrophobic memb:
LSP = endotoxin
-Lipid A = toxic moiety
-PS = immunogenic portion
Outer membrane proteins: attachment, virulence
Protein porins: Passive transport
Teichoic acids present in
Gram (+) only
-immunogenic, induces TNF-alpha, IL-1, attachment
Mycolic acids present in
Acid-fast only
Resistance to drying and chemicals
Periplasmic space present in
Gram (-) only
Endospores present in
Gram (+) only
-Keratin coat, calcium dipicolinate
Resistance to heat, chemicals, & dehydration
What bacterial growth phase:
Initial phase
Detoxifying medium
Turning on enzymes to utilizae medium
Lag Phase
-Number of cells at beginning = number of cells at end of lag phase
What bacterial growth phase:
Rapid exponential growth
Log Phase
-Generation time = time it takes one cell to dividie into two
What bacterial growth phase:
Nutrients used up
Toxic products like acid and alkali begin to accululate
Stationary Phase
-# of new cells = # of dying cells
Medium that selects for certain bacteria by inclusion of special nutrients &/or ABX
Selective medium
Medium on which different bacteria can be distinguished by differences in colonial morphology or color
Differential medium
Thioglycote Medium
Loffler's coagulated and serum (S) and Tellurite agar (D)
Eosin methylene blue (D) and MacConkeys (D)
Enteric Bacterium
Hektoen enteric agar (D) and Xylose-lysine-deoxychocolate agar
Enteric pathogens
TCBS (Thiosulfite Citrate Bile Salts Sucrose agar) (S)
Vibrio cholerae (likes alkaline growth medium)
Charcoal-yeast extract agar (CYE agar) (S)
Lowennstain-Jensen medium (S)
Chocolate agar
Neiserria from normally sterile sites, Haemophilus
Thayer-Martin selective medium (S)
Neiserria from site with normal floar
Cholesterol nd purines and pyrimidines growth requirement
Cysteine growth requirements
Francisella, Brucella, Legionella, Pasteurella
X (protoporphyrin) and V (NAD)
Haemophilus (influenzae and aergypticus require both)
Require oxygen
Have no fermentative pathways
Generally produce superoxide dismutase
Obligate aerobes
-Pseudomonas (Bacillus)
Requires low but not full oxygen tension
Will respire aerobically until oxygen is depleted and then ferment or respire anaerobically
Facultative Anaerobes
-Most bacteria, e.g. Enterobacteriacae
Lack superoxide dismutase
Generally lack catalase
Are fermenters
Cannot use O2 as terminal electron acceptor
Obligate Anaerobes
Types of DNA that may be found in bacteria
Bacterial DNA
Plasmid DNA
Bacteriophage DNA
Where are all essential & nonessential bacterial genes located
Essential : bacterial chromosome
Nonessential: bacterial plasmid
subclass of plasmids
may be integrated into the bacterial DNA
Have insertion sequences matching those found on bacterial chromosomes
2 processes available to stabilize "new" DNA
Homolgous recombination
Site-Specific recombination
mechanism to incorportate short, linear pieces of DNA into the chromosome
must be some sequence homology
recombinase A is required
there is one-to-one exchange of DNA
Homolgous recombination
mechanism used to combine circular pieces of DNA
-Temperate phages
Requires NO homology
No DNA is lost
Requires restriction endonucleases
Site-Specific recombination
3 major roles of Site-Specific recombination
Integration of fertility factor to make an Hfr cell
Integration of temperate phage DNA into a bacterial chromosome to create a prophage
Movement and insertion of transposons
DNA can be transferred from bacterium to bacterium by
How do you get new genetic combinations in bacteria
Gene transfer followed by stabilization of genes (recombination)
What is competent bacteria
capable of binding and importing free DNA from the enivornment
Requires free DNA
Requires competent cells
Captured DNA is incorporated by homologous recombination
Gene transfer from donor (F+ or Hrf cell) to recipient (F- cell) during cell-to-cell contact
What controls conjugation
Fertility factors (in plasmid or episome form)
oriT (origin of transfer)
A single strand break occurs here, this is where transfer of the single strand begins
the other strand remains and it is quickly restored to double strandedness
A plasmid must have this region to be transferrable by conjugation
Donor cells in which fertility plasmid is in its free state
F+ cells
Donor cells in which fertility factor has inserted itself into the bacterial chromosome
Hfr cells
F+ x F- cross
one strand of the entire plasmid is transferred
it results in a "sex change" of the recipient
Hfr x F- cross
Chromosomal genes clostest to oriT are transferred
Transferred genes must be stabilized by homologous recombination
No "sex change" occurs as the bridge does not remain long enough to transfer the tra operon