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CD80 (B7-1) and CD86 (B7-2) are type I transmembrane glycoproteins in the B7 family, belonging to the immunoglobulin superfamily, and are primarily expressed on professional antigen-presenting cells, such as dendritic cells, macrophages, and activated B cells, as well as on activated T cells in certain contexts[2][3][4][8]. These molecules provide critical costimulatory signals required for full T cell activation and survival by binding to the CD28 receptor on T cells; additionally, both CD80 and CD86 interact with the inhibitory receptor CTLA-4 (CD152), which downregulates T cell responses and promotes immune tolerance[1][2][4][5][6]. CD86 is constitutively expressed and rapidly upregulated upon activation, whereas CD80 is more inducible and may play a greater role in sustaining immune responses[6]. The balance of stimulatory (CD28) and inhibitory (CTLA-4) signals mediated by the engagement of CD80 and CD86 is central to maintaining effective immunity while preventing autoimmunity[1][4][5][7]. Therapeutically, these molecules are targeted by biologics for autoimmunity, transplantation, and cancer immunotherapy[7][8].\n\nNotes:\n- CD80/CD86 are not a single receptor or protein, but are commonly discussed together due to their functional redundancy and collaboration in T cell costimulation and coinhibition.\n- Therapies targeting this axis modulate immune checkpoint pathways, fundamental in immune oncology and treatment of autoimmune disorders.
Inhibition of CD80/CD86 interaction with CD28 blocks T cell costimulation, suppressing immune activation (e.g., Abatacept, Belatacept)\nInhibition of CD80/CD86 interaction with CTLA-4 prevents negative regulation, enhancing T cell activation (e.g., Ipilimumab)
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