CMV infection, class II antigen expression, and human kidney allograft rejection.
After successful transplantation, the major histocompatibility complex (MHC) antigens of kidney parenchymal cells are lost and no longer detectable in the graft, presumably due to administration of glucocorticosteroids. During rejection, the MHC antigens reappear in the graft parenchymal cells. The upregulation is possibly due to gamma-interferon released in situ by the allograft activated T (blast) cells. In this communication we demonstrate that cytomegalovirus (CMV) infection is invariably associated with an upregulation of the antigen display in the graft. In 12 of 14 (86%) cases with proved CMV disease, the display of class II antigens was associated with a cytological and/or clinical episode of rejection. In 223 transplant recipients without proved CMV disease transplanted during the same period, the frequency of late rejections was 17% (P less than 0.001). The results suggest that the display of class II antigens on the graft, mediated presumably by gamma-interferon as a consequence of CMV infection, is the reason for graft rejection in context of CMV disease.
D003586:Cytomegalovirus Infections / Q000276:immunology*; D006084:Graft Rejection; D000949:Histocompatibility Antigens Class II / Q000032:analysis*; D006801:Humans; D007371:Interferon-gamma / Q000502:physiology; D007668:Kidney / Q000276:immunology; D016030:Kidney Transplantation; D009393:Nephritis / Q000276:immunology; D013997:Time Factors; D014184:Transplantation, Homologous
D000949:Histocompatibility Antigens Class II; D007371:Interferon-gamma