Abstract
The CD28 and CTLA-4 molecules on T cells and their counterreceptors, B7-1 and B7-2, on antigen-presenting cells constitute an important costimulatory pathway for immune responses to antigen in vitro and in vivo. A primary function of these interactions is to regulate production of T-cell-derived cytokines, including interleukin 2. A soluble form of the CTLA-4 receptor, CTLA4Ig, has been produced which binds B7 with high avidity and functions as a competitive inhibitor of CD28/CTLA-4 interactions. In rodent models, CTLA4Ig inhibits T-dependent antibody responses, blocks organ graft rejection, prevents death from acute graft-versus-host disease, and prevents autoimmune disease. CTLA4Ig has a novel mechanism of action, and also has several attractive features for an immunosuppressive drug, including low toxicity, long serum half-life, and the ability to induce long-lasting antigen-specific immune suppression (tolerance) after therapy. CTLA4Ig thus represents a prototype of a new class of immunosuppressive drugs which function by blocking T-cell costimulation through the CD28 receptor.
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