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Activation of cytotoxic T lymphocytes (CTLs) is a critical process in adaptive immunity, initiated by antigen-presenting cells (APCs) presenting antigens via MHC class I molecules. This activation requires three signals: antigen-specific TCR engagement, costimulatory signals (e.g., CD28-B7), and cytokine signals (e.g., IL-12). Successful activation results in CTL proliferation, acquisition of cytotoxic functions, and targeted killing of infected or malignant cells, playing a crucial role in controlling viral infections, tumors, and other cellular abnormalities. The process is tightly regulated to prevent autoimmunity and excessive tissue damage.
The activation of CTLs involves a three-signal model: (1) TCR recognition of MHC-I-peptide complex, (2) costimulatory signals (e.g., CD28-B7 interaction), and (3) cytokine-mediated signals (e.g., IL-12). This leads to clonal expansion, acquisition of cytolytic machinery, and targeted killing of infected/cancerous cells.
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