CTLA4-Ig PLUS BONE MARROW INDUCES LONG-TERM ALLOGRAFT SURVIVAL AND DONOR-SPECIFIC UNRESPONSIVENESS IN THE MURINE MODEL

Allograft rejection is dependent on T cell activation, which requires both the engagement of the T cell receptor by antigen in the context of the MHC molecule and costimulatory signals delivered by cell surface molecules such as the B7-CD28/CTLA4 pathway. CTLA4-Ig is a fusion protein that blocks this pathway and has previously been shown to prolong both allograft and xenograft survival. The current study demonstrates markedly prolonged murine cardiac allograft survival and specific prolongation of secondary skin grafts using a combination of CTLA4-Ig plus donor bone marrow.