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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.
In turn, this results in the T cell acquiring an activated phenotype seen by the up-regulation of surface markers CD25 +, CD44 +, CD62L low, CD69 + and may further differentiate into a memory T cell. Having adequate numbers of naive T cells is essential for the immune system to continuously respond to unfamiliar pathogens.
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T RM cells develop from circulating effector memory T cell precursors in response to antigen. The main role in formation of T RM cells has CD103 and expression of this integrin is dependent on the cytokine TGF-β. CD8 + effector T cells that lack TGF-β fail to upregulate CD103, and subsequently do not differentiate into T RM cells.
CD2 is a specific marker for T cells and NK cells, and can therefore be used in immunohistochemistry to identify the presence of such cells in tissue sections. The great majority of T cell lymphomas and leukaemias also express CD2, making it possible to use the presence of the antigen to distinguish these conditions from B cell neoplasms.
CD3 (cluster of differentiation 3) is a protein complex and T cell co-receptor that is involved in activating both the cytotoxic T cell (CD8+ naive T cells) and T helper cells (CD4+ naive T cells). [1] It is composed of four distinct chains. In mammals, the complex contains a CD3γ chain, a CD3δ chain, and two CD3ε chains.
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In 1982, Nobel laureate James P. Allison first discovered a clonally expressed T-cell surface epitope in murine T lymphoma. [6] In 1983, Ellis Reinherz first defined the structure of the human T-cell receptor using anti-idiotypic monoclonal antibodies to T-cell clones, complemented by studies in the mouse by Philippa Marrack and John Kappler.