Quiz 2 Immunity Flashcards
Innate immunity pathway
Dendrite/Macrophage’s TLR recognizes PRR/PAMP and stimulated macrophages (phagocytize), inflammatory cytokines (inflammation/shock), and interferons (antiviral)
Adaptive immunity pathway
Dendrite/APC “Eats” and processes an antigen, presenting it on MCH I/II via IL12 & 4 pathway —-> Tcell’s TLR binds MHC I (Th1) or MHC II (Th2) and activates via costimulation from B7 (APC) and CD28 (Tcell) bonding —-> IL-12 pathway differentiates Th1 cells, IL4 pathway differentiates Th2 —-> Th1 uses IL-2 to diff into CD8 (Cytotoxic T cells) and INF-y to diff into macrophages. Th2 uses IL4,5 to diff into B cells, and CD4+T (helper Tcell) initiates Bcell activation via CDL40 (CD4+T) and CD40 (Bcell) binding, CD4+T secretes cytokines to stimulate B cell class switching to change Ig into IgM (aka mature B cells) then B cells can differentiate into plasma cells and make antibodies
B cell activation & class switching
After the naive Tcell differentiates into Th2/CD4+T (via IL-4 pathway) to activate Bcells, it recognizes Bcell’s TLR and makes IL4 (growth) & IL5 (differentiation) factors to make more Bcells —> then CD4+T activates Bcells via CDL40 (T)—–CD40(B) & CD28(T)—-B7(B) Bonds to trigger cytokines from CD4+T to trigger Bcell class switch from Ig to IgM (mature Bcells that can differentiate into plasma cells and make antibodies)
Hapten-Induced Bcell activation
Carrier proteins let haptan’s epitope bind with the hapten-specific IgM on Bcells —-> the epitope interacts with CD4+T’s TLR & Bcell’s MCHII to stimulate more IL4 (Growth) & IL5 (Differentiation) to increase Bcells and antibody-producing plasma cells
Immuno globin structure
2 heavy & 2 light chains are linked via disulfide bonds, and it has a
Fab (fragmented Antibody Binding)= has the variable region, and it determines the isotype (Ig__)
&
Fc (Fragmented Crystallizable) parts, include constant region, carboxyl-terminal, CH2 complement binding site, CH3 site for binding macrophage and neutrophil receptors, confers isotype (Ig____)
Immunoglobulin classes
IgG (H2L2) = Transplacental (mom—> fetus) IgG fixes the compliment, opsonizes the bacteria, then neutralizes the bacterial toxins/viruses. Has subsets Ig1-4 (1 has longest 1/2 life & Is most important)
IgA (H2L2)= Secretions, polypeptides move IgA to mucus membranes and prevent attachment by microbes, serum IgA = x2H2L2, IgA protease disrupts IgA and leaves host vulnerable
IgM= Is active in the primary (immediate) immune response; it’s on Bcells as monomers that act as antigen receptor binding surface receptors. It fixes the compliment. In serum, IgM = pentamer (x5 H2L2 & 10 antigen binding sites) increases its avidity to defend against bacteria/viruses.
- It’s most efficient in AGGN (complement fixation/activation pathways)
- associated with certain fetal infections and cold autoimmune hemolytic anemia
IgE = involved in the immediate hypersensitivity reaction (allergy) because its Fc binds to Mast + Basophils, and IgE cross-links with the antigen (increases serum IgE). IgE also recruited eosinophils to improve the host’s defense against parasites. Lastly, IgE initiates ADCC (Antibody-dependent cellular cytotoxicity)
IgD= not sure yet, but its on Bcells in serum and might be an antigen receptor
Serum vs. Anti-serum vs. Serum sickness
serum = the fluid left over after clotted blood and cells are removed
antiserum = apart of the serum with the highest concentrations of antibodies
serum sickness= multiple injections of serum cause disease and illicit a systemic immune response (type 3 hypersensitivity) against proteins and cause an Arthus reaction (local inflammation at injection site looks like a target) treat with epi/nore epi or die from shock
Consequences of the antigen-antibody binding complex “AC is Always ON All Day, it Costs Alot”
Agglutination= antibodies cause antigens to cluster. (IgM is most efficient)
Opsinization= antibodies coat an antigen and increase chances of being phagocytized.
Neutralization= Antibody binds & blocks the active site on a virus, inactivating it and neutralizing its toxins (IgG is best)
ADCC (antibody-dependent cell-mediated cytotoxicity)= antibodies bind to a larger antigen (parasite) and recruiter eosinophils to destroy it (IgE is best)
Complement activation= antibodies trigger the complement pathway (IgG & M are good)
Bcell class switching is also called
isotype switching
B & T cells that don’t undergo CD28—-B7 bonding are considered
incompetent and anergic (can’t metabolize ATP to function)
MHC I, II, & III
MHC I= HLA A,B,C
MHC II= HLA DQ, DR, DP
MHC III= C2,3 BF
Idiotype vs. Allotype vs. Isotype
Idio = differences in the epitopes of the hypervariable regions of light and heavy chains (increase in diversity of receptors)
Allo = minor differences in the constant regions of the heavy chain (IgG1 —-> IgG4)
Iso = differences in the heavy chains that lead to several antibody classes (class switching)
Affinity vs. Avidity
Affinity = strength of one bond (between the para & epitope), it has high specificity (IgG has high affinity)
Avidity = strength of multiple bonds (IgM is a pentamer and has high avidity but low affinity)
If your patient has recurrent viral infections it means they have
depleted NK cells (NK cells use IgG)
Cell-mediated immunity is also called
type 4 hypersensitivity or DTH (deleted type of hypersensitivity)
Rogue cells cause
nut-dishevelled signaling (uses hosts resources but acts on its own accord)
Positive vs. negative selection (thymic education of Tcells)
Positive= happens in the thymic cortex, it eliminates Tcells that do NOT recognize MHC complexes on our own cells (i.e Don’t recognize self)
Negative = happens in the thymic medulla, it eliminates Tcells that DO recognize our self antigens (this prevents autoimmune reactions aka friendly fire)
What is the role of CD3?
it helps intracellular signaling and activating transcription factors that give rise to the JAK-STAT pathway (produces cytokines)
Graft vs. host disease
immunogens response can be boosted by which drug
penicillin
Winter Bottom sign?
enlarged cervical lymph nodes that might indicate an active infection
Natural killer cells (null cells) are involved in
innate immune response to viruses and cancers, they also double as immune surveillance
and use CD16 (ADCC) & 56 (interact with IgG’s via FC bonding to kill cancer) as biomarkers to differentiate friend from foe
IL1,2,3,4,5,6,7,8,
3 Stages that lead to higher specificity of adaptive immunity in terms of high affinity bonding are
Class-switch recombination—–> somatic hypermutation—–> affinity maturation (this is why our adaptive immunity has a lag period as opposed to our innate defenses)
