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56 Cards in this Set

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To be an effective immune system, it must: (3)
1. Recognize and destroy a diversity of pathogens
2. Recognize effete, altered, or damaged self components
3. Exhibit tolerance to self (avoid autoimmunity)
2 forms of immunity
1. Adaptive
2. Innate
Innate immunity characteristics (2)
1. Provides immediate protection by direct detection of invading microbes
2. Defense response isn't any better or worse every time it sees infection
Adaptive Immunity (4)
1. Adapts to a variety of non-self components
2. Responses to re-infection are faster, better and stronger
3. Develops memory though takes time to develop
4. Can anticipate all possible pathogen derived stimuli
What is Plasma
Remaining stuff after cells centrifuged
What is Serum
Everything gone except fluid
What attracts neutrophils to site of infection and by what process?
chemokines by chemotaxis
Immature form of macrophages
monocytes
Monocytes circulate in:
Macrophages circulate in:
blood
tissue
Professional Phagocytes include (2)
neutrophils, macrophages
Phagocytic process:
1. Microbe adheres to phagocyte
2. Phagocyte engulfs microbe
3. Phagosome fused with lysozome
4. Phagolysozome breaks down microbe
5. Indigestible material released by cell.
What does PMN stand for and give examples.
Polymorphonuclear leukocytes
neutrophils, eosinophils, basophils
Mast cells are a major cause of [ ] because of [ ].

degranualte upon [ ]
allergic symptons because of release of histamine

activation
Natural Killer Cells (3)
Enter infected tissues
Kill infected cells without prior sensitization
Kills cancer cells
Dendritic cells activate:
naive T cells
Dendiritic cells are [ ] [ ] [ ]
Professional Antigen Presenting Cells
Upon maturation which occurs during migration to secondary tissues, dendritic cells:
dendrites become elaborated and d cells become interdigatating d.cells

facilitates extensive interaction with T cells in lymph node
Plasma cells are and do this:
mature/activated B cells and secrete antibodies into the system
B cells originate in the [ ] and migrate to the [ ] and are activated in the [ ] [ ]
bone marrow
seconday lymph tissue/ lymph nodes
germinal center
3 types of T Cells
memory
Helper- encourage macrophage killing
cytotoxic- kill infected target cells
What are PRR and what do they bind

What part of PRR bings sugar?
Pattern recognition molecules and their CRDs (carbo recognition domains) bind terminal sugar residues found on pathogen cell walls (glucose, fucose, mannose, NOT galactose or sialic acid)
Opsonins do what?
coat pathogens in preparation for phagocytosis

encourages macrophage phagocytosis
complement activation leads to (3)
1. Recruitment of inflammatory cells
2. Opsonization of pathogens
3. Killing of pathogens
classical definiton of antigen and examples
any molecule that binds to an antibody or to T Cell receptor and is recognized by that receptor

can be foreign proteins, self proteins (altered) repetitive polymers of polysaccharides
portion of antigen that binds to antibody

how many areas are there on an Antigen?
epitope

they bind with incredibly high levels of specificity (10^15)

mulitple epitopes on the Ag
phagocyte has two receptors for opsonized pathogen. what are they?
Fc receptor for Ab bound Ag and CR for opsonins on pathogen

together they induce phagocytosis better than alone
Antibodies prevent bacterial adherence to cells and activates
complement
Reinfection improves/retards adaptive immune response
improves; T cells have memory for infection
clonal selection theory is:
T Cells that don't recognize self antigens aren't killed. Then APC presents Ag to naive T cells and T cells that match Ag become activated and proliferate and differentiate into mature T cells
Primary Lymphoid tissue
Secondary Lymphoid tissue
Thymus/ Bone Marrow
Lymph nodes, peyer's patches, lymphatic system, etc
Hematopoiesis
Process of blood cell formation
all begin as pluripotent stem cells
differentiation into different cell lines
egress of cells into circulation
B cells/ T cells maturation differences
B cells mature in bone marrow and circulate as mature naive cells
T cells leave bone marrow as immature thymocytes and mature in thymus
B Cell Development issues?
Immature B cell has strong recognition of self antigen, either apoptosis or receptor editing for non-specificity to self antigens

*T cells undergo central tolerance in thymus
Lymphatic system architecture
lymphatic capillaries in tissue space
lymphatic vessels attached to afferent vessels
lymph node in between afferent and efferent vessels *act as tethers during imflammation and vasodilation
3 prinicipal functions of lymphatic system:
1. collect and return interstitial fluid, including plasma proteins to blood, maintain fluid balance
2. absorb lipids from intestine and transport them to the blood
3. defend the host against infectious pathogens by enabling antigen to travel and concentrate in lymph nodes
T cell lymphocyte migration
Naive travel through the blood, into secondary lymphoid tissues, then though efferent lymphatics, then back to blood.
T/F Dendritic cells migrates to Secondary Lymphoid Tissue to present Ag to T cell
True
What is MHC?
Majorhistocompatibility Complex.

a receptor that presents Ag to T cell
MHC molecule
the receptor responsible for presenting peptide antigen to T cells

called Human Leukocyte Antigen in humans
interaction between TCR and MHC-peptide complex takes place:
1. in the thymus during T cell selection
2. in the secondary lymphoid tissues during T cell activation
3. at the site of infection during an immune response
4. all the time during the process of immune surveillance (MHC checks all cells all the time to make sure they are self)
MHC class I
expression, antigen, binding, effectors, function
all nucleated cells, professional APCs
cytoplasmic (virus)
TCR of CD 8+ T cells
Cytotoxic T cells
Kill infected cell
MHC class II
expression, antigen, binding, effectors, function
Professional APCs (only cells that can activate T cells)
Endocytic vesicles
TCR of CD4+ T cells
Helper T cell
Help Macrophages kill
Help B cells make Ab
MHC 1 vs MHC 2 location of pathogen
cystolic pathogens vs endosomal or extracellular pathogens

inside vs outside
the breakdown of proteins and their loading is called
antigen processing
genetic shuffling of loops in TCR causes:
variability in receptor specificity
MHC 1 and 2 protein structure
MHC 1: binds short peptides b/c MHC has pocketed off ends (longer peptides bulge out).
peptide anchored by H bonds
MHC 2: binds longer peptides b/c no pockets on structure
held at constant elevation above floor of MHC cleft (held up in pocket a bit)
MHC class 1 presentation
protein ground up in proteasome
peptides transported by TAP into the lumen of ER
peptide loaded onto MHC
MHC presented on cell surface to TCR of CD8+
Proteasome to Immunoproteasome
IFN gamma induces 3 new subunits to be expressed on proteasome
3 subunits confer specificity for cleavage after hydrophobic and basic residues
= peptides with prefereed binding for MHC 1

occurs during infection and allows more MHC 1 binding to T cells and activation of T cells
What is Tapasin
brings MHC close to TAP proteins and exchanges suboptimal peptides for optimal peptides
MHC class 2 presentation
endocytosed antigens brought to ER and loaded onto MHC peoptide.

complex migrates to cell surface

**endocytosis required for presentation**
MHC class 2 presentation more detailed
RER synthesize MHC 2 bings to invariant chain
bound chain prevents premature binding of peptides to MHC
Digestion of invariant chain leaves CLIP bound groove to MHC groove
HLA-DM takes out CLIP fragment exchanges peptide from pathogen
peptides can bind to MCH 2
Cross presentation
particle bigger than cell injested and ER membrane recruited to help engulf.
SEC 61 breaks down particle and feeds proteins to proteasome
peptides re-enter ER with help of TAP
internal peptides bind to MHC 2 and/or MHC 1
3 CDRs on Vh and Vl regions (Valpha and Vbeta in TCR)
CDR 1 2 and 3
same as hypervariable regions
hypervariable regions (CDRs) placement
lie in discrete loops of the folded structure (Ab or TCR)
Effector functions determined by
constant regions
dimerization of IgE following Allergan binding releases
histamine from mast cell