Long-term survival of xenogeneic pancreatic islet grafts induced by CTLA4Ig

Deborah J. Lenschow, Yijun Zeng, J. Richard Thistlethwaite, Anthony Montag, William Brady, Marylou G. Gibson, Peter S. Linsley, Jeffrey A. Bluestone

Research output: Contribution to journalArticlepeer-review

1089 Scopus citations


Antigen-specific T cell activation depends on T cell receptor-ligand interaction and co-stimulatory 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 (Ig) G1 Fc region (CTLA4Ig) binds to human and murine B7 with high avidity and blocks T cell activation in vitro. CTLA4Ig therapy blocked human pancreatic islet rejection in mice by directly affecting T cell recognition of B7+ antigen-presenting cells. In addition, CTLA4Ig induced long-term, donor-specific tolerance, which may have applications to human organ transplantation.

Original languageEnglish
Pages (from-to)789-792
Number of pages4
Issue number5071
StatePublished - 1992


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