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Interferon-&ggr; is not a universal requirement for islet allograft survival1

Background. Although many transplantation studies have implicated a graft-destructive role for T helper (Th)1 cytokines and a graft-protective role for Th2 cytokines, more recent studies have challenged this paradigm by showing that long-term allograft survival can actually require the presence of Th1 cytokines, such as interleukin 2 and interferon (IFN)-&ggr;. The purpose of this study was to examine the requirement for IFN-&ggr; in the induction of islet allograft acceptance after monoclonal antibody therapy targeting conceptually distinct molecular pathways: the costimulatory molecule CD154, the CD4 coreceptor, or the &bgr;2 integrin lymphocyte function-associated antigen (LFA)-1 (CD11a). Methods. Diabetic C57Bl/6 (B6; H2b) mice were grafted with fully MHC mismatched BALB/c (H2d) islets, or reciprocally, diabetic BALB/c mice underwent transplantation with B6 islets and were treated with anti-CD154, anti-CD4, or anti-LFA-1. Results. When IFN-&ggr; gene knockout mice were used as graft recipients, the requirement for IFN-&ggr; in allograft survival was found to be highly conditional, depending on both the host strain and the induction therapy used. In both strain combinations studied, anti-CD154 was effective in the presence or absence of IFN-&ggr;, whereas anti-CD4 lost therapeutic potential in the absence of this cytokine. Alternatively, the requirement for IFN-&ggr; for allograft prolongation by anti-LFA-1 therapy was noted only in B6 transplant recipients. Conclusions. IFN-&ggr; is not always requisite in islet allograft survival but rather varies according to the molecular target of induction therapy and the genetic background of the transplant recipient.