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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. Activated T cells also change their cell surface glycosylation profile. [49] The T cell receptor exists as a complex of several proteins.
T-cell receptor (TCR) stimulation causes the dephosphorylation of NFAT which in almost every kind of T cell then forms a complex with AP-1 (except in Tregs). This complex depending on the cytokine context then activates the key transcription factors of the distinct T cell subpopulations: T-bet for Th1, GATA3 for Th2, RORγ for Th17 and BATF for ...
In certain circumstances, some activated T cells show a preference for patrolling certain tissues. This has been termed lymphocyte homing. Gut-specific homing is the preferential movement of activated T cells to the intestine and the gut. In this way T cells are effectively recruited to form part of the first line of defense against pathogens ...
The product of this gene is a member of the nuclear factors of activated T cells DNA-binding transcription complex. This complex consists of at least two components: a preexisting cytosolic component that translocates to the nucleus upon T cell receptor (TCR) stimulation and an inducible nuclear component.
In immunology, a naive T cell (T h 0 cell) is a T cell that has differentiated in the thymus, and successfully undergone the positive and negative processes of central selection in the thymus. Among these are the naive forms of helper T cells ( CD4 + ) and cytotoxic T cells ( CD8 + ).
The Linker for activation of T cells, also known as linker of activated T cells or LAT, is a protein involved in the T-cell antigen receptor signal transduction pathway which in humans is encoded by the LAT gene. [5] Alternative splicing results in multiple transcript variants encoding different isoforms. [6]
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Compared to wild-type naïve T cells, ICOS-/- T cells activated with plate-bound anti-CD3 have reduced proliferation and IL-2 secretion. [11] The defect in proliferation can be rescued by addition of IL-2 to the culture, suggesting the proliferative defect is due either to ICOS-mediated IL-2 secretion or the activation of similar signaling pathways between ICOS and IL-2.