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The **T-cell activation process** is a fundamental immunological event whereby T lymphocytes are functionally engaged in response to antigen presentation. Activation requires both signal 1 (antigen recognition by the T-cell receptor interacting with peptide–MHC complex on antigen-presenting cells) and signal 2 (co-stimulatory signals mediated by molecules such as CD28 engaging B7-1/B7-2 on APCs)[3][2]. This process triggers a complex signaling cascade involving protein tyrosine kinases (Lck, Fyn, ZAP-70), adaptor proteins (LAT, SLP-76), and signaling effectors that lead to transcription (NF-κB, NFAT, AP-1) promoting gene expression, cell proliferation, survival, differentiation, and cytokine production[1][4][6]. The immunological synapse, a molecular interface between T cell and APC, is crucial for maintaining and amplifying activation signaling[3][4]. Therapeutically, components of these pathways are targeted in various diseases, especially autoimmunity and transplantation, but direct targeting of the full process is not feasible—as it is not a single molecular entity but a biological ensemble of interactions[3][1].
Blockade of co-stimulatory signals (e.g., CD28/B7 pathway), Antigen recognition inhibition, Depletion of activated T cells, Modulation of downstream signaling pathways (e.g., NFAT, NF-κB, MAPK activation, Ca2+ mobilization)[3][1]
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