IFN-γ blocks CD4+CD25+ Tregs and abolishes immune privilege of minor histocompatibility mismatched corneal allografts.

摘要: Th1 CD4+ cells are believed to be the primary mediators of corneal allograft rejection. However, rejection fully allogeneic C57BL/6 allografts soared from 50% 90% in both interferon-gamma (IFN-γ)(-/-) and anti-IFN-γ-treated BALB/c mice. In contrast, similar deficits IFN-γ hosts enhanced immune privilege BALB.B (minor histocompatibility [minor H] antigen-matched, major complex [MHC]-mismatched) NZB (MHC-matched, minor H antigen-mismatched) allografts-decreasing 80% ~20%. This effect was independent T cell lineage commitment as acceptor rejector mice displayed a Th2 cytokine profile. The presence prevented generation alloantigen-specific CD4+CD25+ regulatory (Tregs) receiving either MHC only mismatched or H)-mismatched allografts. Tregs these promoted survival by suppressing effector cells. By necessary for that hosts. These findings suggest MHC-matching combination with blockade holds promise means enhancing survival.