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Lymphocyte activation gene 3 receptor (**LAG‑3**, also known as **CD223**) is an immune checkpoint receptor expressed on activated T cells and some other immune cells. It functions primarily as an inhibitory regulator of the immune response by delivering negative signals upon binding to its ligands—most notably MHC class II molecules and FGL1—thereby suppressing T cell proliferation, cytokine secretion, and cytotoxic activity. This mechanism helps maintain self-tolerance but can be exploited by tumors to evade the immune system. As a result, LAG‑3 has become a major therapeutic target in cancer immunotherapy; both antagonists that block its function to boost anti-tumor immunity and agonists that enhance its inhibitory effect for autoimmune diseases are under active development. Drugs targeting this pathway include relatlimab (an antagonist antibody), IMP321/eftilagimod alpha (a soluble fusion protein), and GSK2831781 (an agonist antibody). The safety profile is similar to other checkpoint inhibitors with risks related to overactivation or suppression of the immune system depending on the therapeutic approach.[1][2]
Antagonist antibodies block inhibitory signaling to enhance anti-tumor immunity by reactivating effector T cells and inhibiting regulatory T cell suppression.
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