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T lymphocyte and dendritic cell surface receptors refer to a collective group of proteins that facilitate communication between T cells and antigen-presenting cells (APCs) during the immunological synapse (Source: PubMed, PMID: 25324124). This category encompasses the B7-CD28 superfamily, including co-stimulatory receptors like CD28 and their ligands CD80 (B7-1) and CD86 (B7-2), as well as co-inhibitory checkpoint receptors such as CTLA-4 and PD-1 (Source: UniProt, P16410, P33681). These molecules are essential for regulating the magnitude and quality of the T-cell response, ensuring that the immune system can effectively respond to pathogens and tumors while maintaining tolerance to self-antigens (Source: NIH, National Cancer Institute). Pharmacological modulation of these receptors has revolutionized medicine; checkpoint inhibitors like nivolumab and ipilimumab are used to treat various cancers by releasing the brakes on the immune system, whereas co-stimulation blockers like abatacept are used to treat autoimmune diseases like rheumatoid arthritis (Source: StatPearls, Abatacept). However, because these receptors are central to immune homeostasis, their therapeutic manipulation can lead to significant safety concerns, including severe immune-related adverse events (irAEs) and cytokine release syndrome (Source: PubMed, PMID: 29101370).
Modulation of T-cell activation and effector function by targeting co-stimulatory (e.g., CD28, CD80/86) or co-inhibitory (e.g., CTLA-4, PD-1/PD-L1) signaling pathways at the interface between T lymphocytes and dendritic cells.
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