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103 Cards in this Set

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B-Cell site of production and maturation
Production: bone marrow
Maturation: Follicles of lymph nodes
T-cell site of production, maturation, housing and spleen site
Production: bone marrow
Maturation: thymus
Housing: paracortex of lymph node
Spleen site: PALS (periarterial lymphatic sheath)
Drains upper arm, lateral breast?
axillary nodes
Drains stomach
celiac nodeas
drains duodenum/jejunum?
superior mesenteric nodes
drains sigmoid colon
colonic to inferior mesenteric nodes
drains rectum
internal iliac
drains testes
superficial inguinal to PARA-AORTIC nodes
Drains anal canal below pectinate line
superficial inguinal
Drains thigh
superficial inguinal
drains lateral side of dorsum of foot
popliteal nodes
What does right lymphatic duct drain?
right arm and right half of head
What does thoracic duct drain?
Everything else and then goes to IVC
What disease is the paracortex underdeveloped in?
DiGeorge Syndrome
What happens during splenic dysfunction? (sickle cell or trauma)
less IgM so less complement activation so less C3b opsonization so susceptibility for ENCAPSULATED organisms
What are the encapsulated organisms?
S SHiN (salmonella, s. pneumonia, Haemophila influenza, neisseria meningitidis)
Post splenectomy you see?
1) howell-jolly bodies
2) target cells
3) thrombocytosis
Where do + and - selection of lymphocytes occur?
Corticomedullary junction of the thymus
Innate immunity and cell types:
Fast, non-specific, no memory; macrophages, dendritic cells, NK cells (only lymphoid cells), neutrophils and complement
Adaptive immunity and cell types
Slow, specific, memory response is faster and more robust; B-cells, T-cells, circulating antibody
MHC I is expressed on and presents to? what kind of figure?
Almost all nucleated cells (not RBCs); presents to Cytotoxic T cells binding TCR and CD8; mediates viral immunity
large chain and short chain (alpha and beta 2)
MHC II is expressed on and presents to?
what kind of figure?
All antigen presenting cells; presents to T Helper cells by binding TCR to CD4
two large chains (alpha and beta)
Name the 3 types of APCs?
1) Macrophages
2) Dendritic cells
3) B cells
Hemochromatosis HLA?
PAIR: Psoriasis, Ankylosing Spondylitis, Inflammatory bowel dz, and reiter's syndrome
Type 1 Diabetes HLA?
DR3 and DR4
Grave's disease HLA?
Lupus HLA?
Hay fever HLA?
Multiple Sclerosis HLA?
Goodpasture's HLA?
Rheumatoid Arthritis HLA?
Pernicious anemia HLA
Hashimoto's HLA
Steroid responsive nephrotic sydrome
B-Cell functions?
1) make antibody--opsonize bacteria, neutralize viruses
2) activate complement (IgG and IgM)
3) Sensitize mast cells (IgE)
What type of reactions during different organ rejection?
Hyperacute: antibody (B-cell) mediated
Acute and Chronic Organ rejection: T-cell mediated
Positive selection of T cells where and what?
Thymic Cortex: T cells capable of binding surface self MHC survive
Negative selection of T cells where and what?
Corticomedullary junction: T cells with high affinity for self undergo apoptosis; want some recognition, but without attack
Helper T-cell activation
1) phagocytosis of foreign body by APC
2) presentation on MHC II to Th (signal 1)
3) CD7 costimulation by linking with CD28 (signal 2)
4) Release of cytokines
Cytotoxic T-cell Activation
1) Endogenously synthesized viral or self proteins are presented on an MHC I cell to a CTL via CD8 (signal 1)
2) IL-2 from a Th cell signals T-cell to kill (signal 2)
B-cell activation and class-switching
1) Helper T activation
2) Receptor mediated endocytosis
3) IL-4, 5, 6 from Th2 (signal 1)
4) CD 40 receptor on B-cell binds CD40 ligand on Th2 (signal 2)
5) costimulation from B7 and CD28
1) Regulates
2) Secretes
3) Activates
4) Is inhibited by?
1) Cell-mediated response
2) IFN-gamma and IL-2
3) macrophages and Cytotoxic T-cell
4) IL-10 from Th2
1) Regulates
2) Secretes
3) Activates
4) Is inhibited by?
1) Humoral Response
2) IL-4,5 and 10
3) B-cells to make antibody
4) IFN-gamma from Th1
Cytotoxic T-cells kill what via what?
Virus-infected cells, neoplastic cells and donor graft cells via apoptosis (granzyme and perforin)
Fab region?
2 heavy and 2 light chains, binds antigen
Fc region of antibody?
Constant, carboxyl terminal, complement binding, Determines Isoptype
How is antibody diversity generated?
1) Recombination of V, J light chain and V D, J heavy chain genes
2) random combination of heavy chains with light chains
3) somatic hypermutation
IgG Details?
1) Main antibody in 2ndary (delayed) response
2) Fixes complement, opsonizes bacteria, neutralizes bact toxins and viruses
3) can cross the placenta
4) most prevalent antibody in blood
1) Found in secretions
2) monomer in circulation
3) dimer when secrested
1) IMMEDIATE response to antigen
2) Fixes complement, but doesn't cross placenta
3) monomer on b-cell
4) pentamer (helps trap free antigens)
1) binds mast cells, basophils which release histmine
2) hypersensitivity type 1
3) least amount of any immunoglobulin
Viral neutralization performed by?
C1, C2, C3, C4
Opsonization performed by?
Anaphalaxis performed by?
C3a, C5a
Neutrophil chemotaxis via?
Cytolysis by MAC
What inhibits complement?
1) Decay-accelerating factor (DAF)
2) C1 Esterase inhibitor
Activation of the Classic pathway (C1, C2 and C4) is mediated by?
IgG and IgM (antibody-antigen complexes)
Activation of the Alternative pathway (C3) is mediated by?
Microbe Surface molecules (endotoxin, etc)
C1 esterase inhibitor deficiency
hereditary angioedema (ACE inhibitors are contraindicated since more bradykinin)
C3 deficiency
Severe recurrent pyogenic sinus and respiratory tract infections
C5-C8 deficieny:
Recurrent neisseria bacteremia
DAF deficiency
complement-mediated lysis of RBCs and PNH
IL-1: Fever
IL-2: T-Cell stimulator
IL-3: Stimulates Bone Marrow
IL-4: Stimulates IgE production
IL-5: Stimulates IgA production
What cytokines are secreted by macrophages?
IL-1, Il-6, IL-8, IL-12, TNF-alpha
Causes fever and acute inflammation; induces chemokine secretion to recruit leukocytes
Fever and production of acute-phase proteins
Major chemotactic factor for neutrophils
1)Induces differentiation into Th1 cells
2) activates NK cells
3) deficiency leads to recurrent mycobacterium infection
1) Mediates septic shock
2) Leukocyte recruitment/vascular leak
3) secrete by macrophages
What is secreted by all T cells? Th1? Th2?
All: IL-3
Th1: IFN-gamma, IL-2
Th2: IL-4, IL-5, IL-10
Growth and differentiation of Bone Marrow stem cells (like GM-CSF)
Stimulates T-cell production (both kinds)
1) activates macrophages and Th1 cells
2) suppresses Th2 cells
3) Anti-viral and anti-tumor properties
1) Induces differentiation to Th2 cells
2) class switching to IgE and IgG
1) differentiation of B-cells
2) Class switching to IgA
3) Eosinophil production
1) Inhibits Th1
2) Activates Th2
3) TGF-B is similar since they both INHIBIT INFLAMMATION
Interferon Mechanism?
Induce the production of a ribonuclease that inhibits viral but not host protein synthesis by degrading viral mRNA
Cell Surface proteins on all T cells? T-helper? Cytotoxic t?
All: CD3, TCR, CD28
T-helper: CD4
Cytotoxic: CD8
B-cells cell surface proteins:
Ig, CD19. CD20, CD21 (EBV receptor), CD40, B7, MHC II
CD14, CD40, MHC II, B7, Fc, C3b
NK Cells:
CD16, CD56
All cells (except mature red cells) have this cell marker?
What is anergy?
Self-reactive T-cells become non-reactive w/o costimulatory molecule
How do superantigens get consumed?
Cross-link TCR to MHC II on APCs releasing IFN-gamma from Th1 and subsequent cytokines from macrophages
How do Endotoxins/lipopolysaccharide on gram neg bacteria get consumed?
directly stimulate macrophages by binding to endotoxin receptor CD14
Passive Immunity:
1) means of acquisition?
2) onset
3) duration
4) examples
1) receiving preformed antibodies
2) Rapid
3) Short span (3-weeks)
4) IgA in breast milk, antitoxin, humanized monoclonal antibody
After exposure to which diseases should you be given preformed antibodies "to be healed rapidly?"
tetanus toxin, botulinum toxin, HBV, Rabies (RSV for premies)
Active Immunity:
1) means of acquisition?
2) onset
3) duration
4) examples
1) Exposure to foreign antigens
2) slow
3) long
4) natural infections, vaccines, toxoid
Pros/cons of live attenuated vaccine? Examples? Type of reaction it invokes?
Pros: strong life-long immunity
Cons: may revert to virulent
Examples: Sabin, MMR, VSV, Yellow Fever
Type of rxn: Cellular response (t cells)
Pros/cons of killed vaccine? Examples? Type of reaction it invokes?
Pros: stable and safer
Cons: Need booster
Examples: Salk, Rabies, Cholera, HepA, influenza
Type I Hypersensitivity Mechanism?
1) Anaphylatic and atopic
2) IgE on mast cells and basophils; release of histamine
3) Scratch test (wheel and flare)
4) hives/asthma
Type II Hypersenstivity Mechanism?
1) Antibody mediated: IgM, IgG bind to fixed antigen on enemy cell leading to lysis by complement (MAC) or phagocytosis
2) Test: direct and indirect coomb's
3) disease often specific to site where antigen is found
Type III Hypersensitivity:
1) Immune-complex (antibody-antigen-complement stuck together...3 things) activate complement which attracts neutrophils
2) Serum sickness (now caused by drugs)
3) Arthus reaction
4) Test: immunofluorescent staining
5) often vasculitis and systemic involvement
What is serum sickness?
A type III hypersensitivity rxn now caused by drugs resulting in fever, lymphadenopathy, urticaria, arthralgias and proteinuria 5-10 days after exposure; immune complexes are deposited in membranes where they fix complement
What is the Arthus Reaction?
A type III hypersensitivity where intradermal injection of antigens induces antibodies which form complexes in skin.
Characterized by edema, necrosis and activation of complement
Type IV Hypersensitivity:
1) Delayed (T-cell mediated) type
2) T-lymphocytes encounter antigen and release lymphokines leading to macrophage activation (no antibody involved)
3) 4T's: T-lymphocytes, Touching (contact dermatitis), TB testing, Transplant rejection
4) Test: path test
Pneumonic for Hypersenstivity?
Anaphylatic and atopic
Immune Complex
Delayed (cell mediated)
Allergic Blood Transfusion Rxn
Type I reaction against plasma proteins;
Urticaria, pruritis, wheezing, fever
Anaphylatic Blood Transfusion Rxn
SEVERE, IgA deficient people MUST receive blood that lacks IgA
Dyspnea, bronchospasm, hypotension, resp arrest, shock
Febrile Nonhemolytic Transfusion Rxn
Type II hypersenstivity; host antibodies again HLA antigens
Fever, flushing, headaches, chills
Acute hemolytic transfusion Rxn (HTR)
Type II; Intravascular (ABO incompatability) or Extravascular (foreign antigen) hemolysis
Fever, jaundice, flank pain, tachypnea, tachycardia, hemoglobinemia