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In the thymus, where T cells mature, it prevents autoimmune diseases by promoting the differentiation of certain immature T cells into regulatory T cells, which suppress other T cells that are otherwise primed to attack normal healthy cells in the body. IL-2 enhances activation-induced cell death (AICD). [5]
[19] [20] High expression of CD25 is also found on TCR activated conventional T cells (both CD8+ and CD4+ T lymphocytes), where it is considered to be a marker of T cell activation. [21] Additionally, expression of the IL-2 receptor alpha subunit can be found in non-lymphoid tissues such as lungs ( alveolar macrophages ), liver ( Kupffer cells ...
Interleukin 10 (IL-10) is a protein that inhibits the synthesis of a number of cytokines, including IFN-gamma, IL-2, IL-3, TNF, and GM-CSF produced by activated macrophages and by helper T cells. In structure, IL-10 is a protein of about 160 amino acids that contains four conserved cysteines involved in disulphide bonds. [33]
The autocrine or paracrine secretion of IL-2 can bind to that same T h cell or neighboring T h 's via the IL-2R thus driving proliferation and clonal expansion. The T h cells receiving both signals of activation and proliferation will then become T h 0 (T helper 0) cells that secrete IL-2, IL-4 and interferon gamma (IFN-γ).
Activation of T cells without co-stimulation may lead to the unresponsiveness of the T cell (also called anergy), apoptosis or the acquisition of the immune tolerance. [ 3 ] The counterpart of the co-stimulatory signal is a (co-)inhibitory signal, where inhibitory molecules interact with different signaling pathways in order to arrest T cell ...
These cytokines mediate the activation of type 2 T helper cells (T h 2 cells), type 2 innate lymphoid cells (ILC2 cells), and dendritic cells. T h 2 cells and ILC2 cells secrete IL-4, IL-5 and IL-13. [1] [3] IL-4 further drives CD4+ T cell differentiation towards the T h 2 subtype and induces isotype switching to IgE in B cells. IL-4 and IL-13 ...
Markers of T cell activation include CD69, CD71 and CD25 (also a marker for Treg cells), and HLA-DR (a marker of human T cell activation). CTLA-4 expression is also up-regulated on activated T cells, which in turn outcompetes CD28 for binding to the B7 proteins. This is a checkpoint mechanism to prevent over activation of the T cell.
Once IL-2 binds to the high affinity receptor, the complex is rapidly internalized and has only a short time to signal. IL-2, IL-2Rβ, and γ c are rapidly degraded, but IL-2Rα is recycled to the cell surface. Thus, the concentration of IL-2 and its receptor available determines the tempo, magnitude and extent of T cell immune responses. [3] [4]
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