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CD80 (B7-1) and CD86 (B7-2) are critical costimulatory molecules expressed on the surface of professional antigen-presenting cells (APCs), such as dendritic cells, macrophages, and B cells [1, 11]. They serve as ligands for the CD28 and CTLA-4 receptors on T lymphocytes, providing the essential second signal required for full T-cell activation, proliferation, and survival following antigen recognition [2, 7]. While CD86 is constitutively expressed and rapidly upregulated, CD80 is typically induced later during the immune response [7, 11]. Dysregulation of the CD80/CD86 pathway is implicated in various autoimmune conditions, such as rheumatoid arthritis and systemic lupus erythematosus, as well as in transplant rejection [3, 8]. Therapeutic agents like abatacept and belatacept are fusion proteins that bind to CD80 and CD86, effectively blocking their interaction with CD28 and inducing T-cell anergy [1, 5]. This modulation of the costimulatory pathway is a key strategy for managing immune-mediated diseases and improving outcomes in organ transplantation [2, 4].
Selective T-cell costimulation modulation via competitive inhibition of CD28 binding to CD80 and CD86
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