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IgG
can cross placenta & aids in complement activation, toxin neutralization, opsonization for phagocytosis
Main one
IgA
Agglutination of antigens & found commonly in mucosal membranes/tears
IgE
binds surface receptors of mast cells & basophils
IgM
1st antibody made in primary immune responseD
Different ways antibodies help
agglutination - create larger target of viruses
prevent binding of pathogen
neutralize toxin
Opsonization - Fc portion of antigen binds to FcR of phagocyte (more efficient process)
activate complement proteins
Specificity of adaptive immune system
TCR & BCR/antibodies can only bind specific epitopes
Unresponsiveness to self of adaptive immune system
B & T cells undergo positive & negative selection to make sure they do are functioning properly (each one in its respective maturation areas)
positive selection - cell has activity & if no activity then apoptosis (testing if functional)
negative selection - cell must NOT have activity & if does then apoptosis (testing if reacts to self or not)
Where do mature naive b/t cells go?
blood stream circulating body and not concentrated in specific organs
b cells mature in
bone marrow
t cells mature in
thymus
clonal deletion
getting rid of self-reactive cells
Inducibility/clonality of adaptive immune system
TCR/BCR binds epitope it is specific for = activated
naive = not met their antigen yet
T cells must have their antigen presented by MHC on professional APC
True
mhc 1 presents
endogenous antigens & interact with CD8
found on ALL cells
mhc 2 presents
exogenous antigens & interact with CD4
only on professional APCs
professional antigen presenting cells
dendritic cells (not good at killing but uptake yes & main purpose = antigen presenting)
b cells
macrophages (good killers)
naive cd4 T-cells become
effector helper T cells (TH)
naive cd8 T-cells become
effector cytotoxic cells (TC)
IL-2 cytokine
proliferation & differentiation of T-cells
How is activation different between helper and cytokine t-cells?
helper t-cells can self activate bc IL-2 & IL-2R are both on cell but cytokine t-cells need IL-2 from helper t-cell to become activated
Cytotoxic t-cells (Tc) kill infected host cells same as NK cells which is by
releasing perforin (creates pores in membrane) and granzymes (induces apoptosis)
what is difference between NK & Tc?
in absence of MHC1 —> NK kill cell
In interaction of MHC 1 —> Tc kills cell
in order to induce expansion & differentiation B-cells must get help from
helper t cells
can b cells present any antigen like the other 2 professional APCs (dendritic and macrophages)?
NO only b cell receptor antigens
process of activation of b cell
first step
antigen binds to BCR (b cell receptor) and is endocytosed
b cell activation step 2
antigen is then presented on MHC 2 molecules s
step 3 - b cell activation
antigen on mhc II interacts with cd4 on helper t cell & t cell releases cytokines to activate expansion & differentiation of b cells
which cytokines are important for b cell expansion and differentiation
IL-4, IL-5, IL-13
a humoral immune response from the adaptive immune system is
antibody mediated — more for extracellular infections
a cell-mediated immune response from the adaptive immune system is
cytotoxic t-cell mediated — more for intracellular infections (viral infections)
which helper t-cell is associated with a humoral response of the immune system?
TH2
which helper t-cell is associated with a cell-mediated response of the immune system?
TH1
cytokine TFN-alpha and interferon-gamma (IFN-gamma) are
pro-inflammatory cytokines & stimulate macrophages
IFN-alpha/beta
produce a generalized antiviral state in infected cells and uninfected neighboring cells, which protects them from viral infection
IL-2
clonal expansion & differentiation of t-cells
IL-4, IL-5, IL-13
clonal expansion & differentiation of b-cells
attenuated vaccine is
live virus but not virulent (sabin)
cross-presentation
exogenous antigens taken up by phagocytosis/endocytosis & presented by MHC (1 instead of MHC 2) —> activate naive cd8 t-cells (cytotoxic t-cells)