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21 Cards in this Set
- Front
- Back
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T-cell receptors (TCR)
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-variable and constant regions
-alpha and beta chains -somatic recombinations -only one antigen-binding site |
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Th cell
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-have CD4 surface molecules
-bind to MHC2 on APC cells -secrete cytokines |
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Tc cell
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-have CD8 surface molecules
-bind to MHC1 on cells -secrete perforin (apotosis) and granzymes -job: kill cells |
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Th cell is activated by:
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1. TCR bind to MHC2+ antigen
2. CD4 +MHC2 3. co-stimulatory peptide B7(CD80) +CD28 -B7: produced by PAMP+TLR on APC [all of these are required for Th cell to activate] |
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Tc cell activated by:
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1. TCR bind to MHC1+antigen
2. CD8 + MHC1 3. CD28 +B7 on APC or 4. cytokine (IL-2) from activated Th cells |
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Tc cell gets more activated to the :
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non-infected cell surrounded by infected cells
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co-stimulatory B7 is produced :
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PAMP+PRR (phagocyte)
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B cell activated by:
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-BCR + antigen
-Th cell receptor recognizes antigen at least epitope on B cell's MHC2 [if both don't occur B cell becomes anergic] |
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"activation" of T cell is via:
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phosphorelay second-messenger system
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ex. of phosphorelay second-messenger system
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sensor kinase+TCR -> triggers response regulator by phosphorelation-> transcribe genes-> trigger cytokine
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activated Tc cell function:
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-TCR binds to cell with "correct" antigen on its MHC1
-"correct": same antigen that Tc cell's TCR recognized when it was activated (can't be self antigen) -release cytotoxin (perforin, granzymes) -apotosis -release cytokines to help stimulate nearby macrophages |
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phagocyte produces B7 cell when:
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only it engulfs a foreign antigen
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why not self-antigen:
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-self-recognizing antigens get clonally deleted
-unless there is an infection nearby, Tc cell won't be activated since nonAPCs don't produce a second signal for activation (B7) |
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activated Th cell function:
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1>stimulate proliferate and differentiate of B cell that
engulfed T-dependent antigen 2>bind to MHC2 of macrophage and secrete cytokines that boost macrophage response -more lysosomes -nitric oxide added to oxidative burst: make macrophages more like phagocyte -giant cells +granulomas form: only happens when your cell can't kill bacteria |
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3>autostimulatory cytokines cause the Th cell to
proliferate-clonal selection (just like for B cell) -memory T cells: long lived, can be reactivated just by binding antigen -Treg cell: reduce the T cell response (when the infection is over, or in the gut esp. large intestine), this is for not to over-stimulate the immune response, strong enough that it doesn't need not signals to be activated |
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Treg cells are important modulators of the immune response:
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1. produce anti-inflammatory IL-10
-signals that reduce expression of stimulatory cytokines from Th cells -esp. in the gut 2. destabilize low-affinity DC-Tc cell interaction -allows only specific recognition of non-self antigen 3.produced CTLA-4 (CD152) -reduces the secretion of IL-2 from Th cells -removes B7 from surface of APC by endocytosis |
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T cells undergo clonal deletion too:
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1. occurs in thymus
2. 95% of t cells are selected against |
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positive selection:
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1. T cells must bind to MHC1 in the thymus to be
stimulated to develop 2. T cells that fail to recognize MHC could never function-are left to die |
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negative selection:
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1. T cells must NOT bind to antigen on MHC1 (a self
antigen) 2. if they do, the binding is too tight for them to be released to the circulation |
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NK cells:
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1. bind to vaccenic acid on bacterial surface
2. bind to Fc part whose Fab parts are bound to a bacterium (ADCC) 3. bind to "stress sensor"(kill signal) on any other cell -if MHC1 is also present, kill signal is cancelled -cancer and virus-infected cells often down- regulate MHC1 or up-regulate stress signals, so they fail to cancel the kill signal |
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A cancer vaccine that has recently passed phase I clinical trials uses adenovirus genetically engineered to carry the B7 gene. How would this "vaccine" work?
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enhance the activation of T cells by nonAPCs
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