CD28/B7 Costimulation: A Review - PubMed

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Abstract

The current model of T cell activation requires two signals. The first signal is specific, requiring T cell receptor recognition and binding to MHC/Antigen presented by an antigen-presenting cell. The second signal is nonspecific, resulting from the binding of B7 ligand on the antigen-presenting cell with its receptor, CD28, on the T cell. If both signals are provided, the T cell will proliferate and secrete cytokines. Recently, it has been shown that CTLA4, another receptor for B7 that is upregulated following T cell after activation, can deliver an inhibitory signal, downregulating T cell proliferation. The B7 family of ligands has two family members, B7-1 and B7-2. They both bind to CD28 and CTLA4, but they differ in their binding affinity, structure, and temporal expression. Considerable research has been done on the CD28/B7 costimulatory pathway. Different ways of manipulating this pathway could provide insights into the mechanism and treatment of opposing pathological states. Blocking the CD28/B7 pathway could result in immunosuppression, with implications for the treatment of autoimmune diseases, organ transplantation, and graft vs. host disease. Activating the CD28/B7 pathway could be useful for including the immune system to recognize and eliminate tumors that evade the immune system. Finally, the CD28/B7 pathway could be involved with maintaining immune tolerance, as recent studies suggest the preferential binding of the B7-CTLA4 pathway results in the down-regulation of the responding T cells. Thus, the B7/CD28/CTLA4 pathway has the ability to both positively and negatively regulate immune responses.

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• B7-CD28 interaction is a late acting co-stimulatory signal for human T cell responses. Zhang YQ, Joost van Neerven RJ, Van Gool SW, Coorevits L, de Boer M, Ceuppens JL. Zhang YQ, et al. Int Immunol. 1997 Aug;9(8):1095-102. doi: 10.1093/intimm/9.8.1095. Int Immunol. 1997. PMID: 9263006
• The complexity of the B7-CD28/CTLA-4 costimulatory pathway. Schweitzer AN, Sharpe AH. Schweitzer AN, et al. Agents Actions Suppl. 1998;49:33-43. doi: 10.1007/978-3-0348-8857-8_6. Agents Actions Suppl. 1998. PMID: 9426826 Review.
• The B7-CD28/CTLA-4 costimulatory pathways in autoimmune disease of the central nervous system. Anderson DE, Sharpe AH, Hafler DA. Anderson DE, et al. Curr Opin Immunol. 1999 Dec;11(6):677-83. doi: 10.1016/s0952-7915(99)00036-9. Curr Opin Immunol. 1999. PMID: 10631554 Review.
• Absence of B7-dependent responses in CD28-deficient mice. Green JM, Noel PJ, Sperling AI, Walunas TL, Gray GS, Bluestone JA, Thompson CB. Green JM, et al. Immunity. 1994 Sep;1(6):501-8. doi: 10.1016/1074-7613(94)90092-2. Immunity. 1994. PMID: 7534617
• CTLA-4-B7 interaction is sufficient to costimulate T cell clonal expansion. Wu Y, Guo Y, Huang A, Zheng P, Liu Y. Wu Y, et al. J Exp Med. 1997 Apr 7;185(7):1327-35. doi: 10.1084/jem.185.7.1327. J Exp Med. 1997. PMID: 9104819 Free PMC article.

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