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Activation of CD4+ helper T lymphocytes describes the process whereby naive CD4+ T cells are triggered through engagement of their T cell receptor (TCR) with antigen presented via major histocompatibility complex II (MHC-II) on antigen-presenting cells, together with costimulatory signals such as CD28 engagement and a cytokine milieu that directs differentiation[1][2][5][6][7]. This activation leads to proliferation and differentiation of CD4+ T cells into various subsets (Th1, Th2, Th17, Tfh, Treg, etc.), each orchestrating distinct arms of the immune response through cytokine production, B cell help, and regulation of cytotoxic T cell responses[5][7]. Co-inhibitory molecules, metabolic switches, and finely tuned intracellular signaling cascades regulate the magnitude and quality of the response, and dysregulation at any step can contribute to autoimmunity, immune deficiency, or cancer[1][2][6][7].
Inhibition of costimulatory signaling (e.g., abatacept); Suppression of T cell receptor signal transduction (e.g., calcineurin inhibitors block NFAT signaling); Depletion or modulation of T cells (anti-CD3 therapy)
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