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Cytotoxic T‑lymphocyte associated protein 4 receptor (CTLA‑4) is an inhibitory immune checkpoint receptor expressed primarily on activated and regulatory T cells. It is a type I transmembrane glycoprotein belonging to the immunoglobulin superfamily. Upon binding its ligands CD80 or CD86 on antigen-presenting cells with high affinity, it transmits an inhibitory signal that downregulates early stages of T cell activation. This function serves as a critical brake on adaptive immunity to maintain self-tolerance and prevent excessive immune responses. Therapeutically targeting CTLA‑4 with monoclonal antibodies releases this inhibition, enhancing anti-tumor immunity but also increasing risk for autoimmune side effects.
Drugs such as ipilimumab block the interaction between CTLA‑4 and its ligands (CD80/CD86), thereby preventing inhibitory signaling. This enhances T cell activation and proliferation, boosting anti-tumor immune responses.
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