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MUA M2B2 IDR 03.5
Adaptive immune regulation pt. 2
Term | Definition |
---|---|
ITIM immunoreceptor tyrosine-based inhibition motif | part of inhibitor Fc receptor |
Hybridomas | grow at the rate of myeloma cells , also produce large amounts of the desired antibody |
HGPRT (Hypoxanthine-guanine phosphoribosyltransferase) | an enzyme that allows cells to grow on a medium containing HAT (hydroxanthine, aminopterin, and thymidine). |
Only______can live in the HAT medium | hybridomas- unfused myeloma cells and spleen cells die |
Secondary responses are the result of | activation of memory lymphocytes |
Primary immune response lead by | IgM |
Secondary immune response leady by | IgG |
B-cell–specific activator protein (BSAP) | as a master B-cell regulator. BSAP also influences the final differentiation events leading to the formation of memory B cells and plasma cells. Plasma cells do NOT express BSAP. |
The heavy-chain 3’α enhancer (E3’α) | contains binding sites for several transcription factors. Binding of BSAP to __appears to influence B-cell development by preventing the binding of other transcription factors. |
BSAP levels are high | This factor appears to block binding of NF-αP to the 3’α enhancer (E3’α), thereby blocking transcription of the heavy-chain gene and promoting formation of memory B cells. |
When BSAP levels are low | NF- αP can bind to E3’α. Transcription of the immunoglobulin heavy-chain gene ,formation of plasma cells. |
Tissue-resident memory T cells | persist in previously inflamed tissue and function as first responders to cognate antigen re-exposure. |
circulating memory T cells | augment inflammation by rapidly migrating to inflamed tissue or responding to cognate antigen within secondary lymphoid organs and producing additional effector T cells. |
T(Central Memory) express high levels of | CD62L and CCR7, tend to be found in the lymph nodes and tonsils, and have higher proliferative ability. |
CD62L- and CCR7-low | TEffectorMemory cells tend to be found in the lungs, gut, and liver and have more potent effector function. |
CTLA-4 (CD152) is an essential checkpoint control for | T cell response |
(CTLA-4), which is expressed on T cells only | AFTER T-cell activation. |
CTLA-4 is similar to CD28 and binds to | B7 (CD80 and CD86) molecules with much higher affinity than CD28. |
with anti-CTLA-4 antibodies | blocks this inhibitory interaction and CD28 is again free to interact with the B7 molecules, further amplifying T cell responses against the appropriate target. |
IL-2 is produced by | activated T cells and acts back on these cells to produce more IL-2 and IL-2 receptor. Causes T, B and NK cell proliferation, also NK activation |
Either the CD4+ or the CD8+ subsets possess few high-affinity | IL-2 receptors. |
IL-2 binds to and signals through a receptor complex consisting of | three distinct subunits designated as:IL-2Rα (CD25), IL-2Rβ (CD122), and common γ -chain (CD132). |
IL-4 | icreases MHC class II antigens on B-cells and makes them more responsive. Encourages B cell isotype switching to IgE, Differentiates Th2 cells |
INFy is produced by | activated T lymphocytes (TH1 and CD8+ cells), NK cells, B cells, NKT cells and professional APCs. |
IFN-γ stimulates | the cytolytic activity of NK cells. Activates vascular endothelial cells, promoting CD4+ T lymphocyte adhesion and morphological alterations, which FACILITATES lymphocyte EXTRAVASATION. |
TGF-β | inhibits the proliferation of B-lymphocytes (IL-2), proliferation of thymocytes (IL-1), inhibits maturation of B cells, suppresses cytotoxic activity of NK cells (IFN), activity of cytotoxic T-lymphocytes, proliferation of the precursors of LAK cells |
All the antibodies secreted by a single plasma cell have the same isotype | True |
When boosters are administered at intervals for tetanus toxoid, B lymphocytes would have | surface IgG, IgA or IgE |