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Immune cell surface receptors are a broad and heterogeneous class of membrane-bound proteins expressed on leukocytes that facilitate communication between the immune system and its environment (Murphy & Weaver, 2016). These receptors, which include the immunoglobulin superfamily, Toll-like receptors, and cytokine receptors, are responsible for recognizing antigens, sensing inflammatory signals, and regulating the magnitude of the immune response (Janeway et al., 2001). They play a dual role in human health: while essential for defense against pathogens and malignancy, their dysregulation is a primary driver of autoimmune diseases and chronic inflammation (Zola et al., 2007). In the pharmaceutical industry, these receptors are among the most highly prioritized targets, with therapies ranging from monoclonal antibodies that block inhibitory checkpoints to restore anti-tumor immunity to antagonists that suppress overactive cytokine signaling (Pardoll, 2012). Because these receptors are central to systemic homeostasis, therapeutic intervention often requires a delicate balance to avoid severe side effects such as cytokine release syndrome or broad immunosuppression (Postow et al., 2018).
Drugs targeting immune cell surface receptors typically act by blocking inhibitory signals (checkpoint inhibitors), neutralizing circulating ligands, inducing cell depletion through antibody-dependent cellular cytotoxicity (ADCC), or activating stimulatory pathways to enhance immune surveillance (Pardoll, 2012; Weiner, 2015).
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