Alpha Omega Alpha Honor Medical Society

2012 Research Abstract

Critical role of Type I NKT Cells in Posttransplant Alloantibody Production

Investigator: Prashanth Swamy, The Ohio State University College of Medicine

Mentor: Ginny Bumgardner, MD, PhD,Department of Surgery, Comprehensive Transplant Center, The Ohio State University College of Medicine

Mechanisms behind humoral alloimmunity are important to understand in order to prevent rejection after transplantation. This lab has previously reported that maximal posttransplant alloantibody production is IgG1 isotype dominant, driven by IL-4+CD4+ T cells and inhibited by IFN-γ+CD8+ T cells. I hypothesized that IL-4 producing type I NKT cells are also critical for maximal posttransplant alloantibody production. To investigate this hypothesis, alloantibody levels were examined in CD8-deficient wild-type, CD1d KO (NKT cell-deficient), and Jα18 KO (type I NKT cell-deficient) hepatocyte transplant recipients. Analyses showed that the number of IgG1 alloantibody-producing B cells and the magnitude of IgG1 alloantibody were critically dependent on the presence of type I NKT cells. Unexpectedly, alloantibody enhancement was independent of IL-4-production by NKT cells. This is the first report detailing a novel role for type I NKT cells in enhancing posttransplant alloantibody production in response to endogenous antigenic stimuli. These findings may help in the development of more targeted immunosuppressive therapies that inhibit the magnitude of alloantibody production, thus prolonging graft and patient survival.

Updated on August 7, 2013.

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