Bivalent CTLA4 homodimers bridge bivalent B7.1 homodimers to form an unusually stable signaling complex. Blocking B7/CD28 interactions with monoclonal antibodies or soluble receptors results in immunosuppression and enhanced allograft survival, while B7/CTLA-4 blockade results in enhanced antitumor immune responses. The interaction of co-stimulatory molecules on T cells with B7 molecules on antigen presenting cells plays an important role in the activation of naive T cells. Consequently, agents that disrupt these interactions should have applications in treatment of transplant rejection as well as autoimmune diseases[1].
Kinase Assay
Cell Assay
Animal Administration
References
[1]. Green NJ, et al. Structure-activity studies of a series of dipyrazolo[3,4-b:3',4'-d]pyridin-3-ones binding to the immune regulatory protein B7.1. Bioorg Med Chem. 2003 Jul 3;11(13):2991-3013.
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