Long-Term Survival of Xenogeneic Pancreatic Islet Grafts Induced by CTLA4lg
Deborah J. Lenschow(May Institute), Yijun Zeng(University of Chicago), J. Richard Thistlethwaite(University of Chicago), Anthony Montag(University of Chicago), William Brady(Bristol-Myers Squibb (United States)), Marylou G. Gibson(Bristol-Myers Squibb (United States)), Peter S. Linsley(Bristol-Myers Squibb (United States)), Jeffrey A. Bluestone(May Institute)
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Abstract
Antigen-specific T cell activation depends on T cell receptor-ligand interaction and costimulatory signals generated when accessory molecules bind to their ligands, such as CD28 to the B7 (also called BB1) molecule. A soluble fusion protein of human CTLA-4 (a protein homologous to CD28) and the immunoglobulin (lg) G1 Fc region (CTLA4lg) binds to human and murine B7 with high avidity and blocks T cell activation in vitro. CTLA4lg therapy blocked human pancreatic islet rejection in mice by directly affecting T cell recognition of B7+ antigen-presenting cells. In addition, CTLA4lg induced long-term, donor-specific tolerance, which may have applications to human organ transplantation.
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