Murine Graft-Versus-Host Disease in an F 1 -Hybrid Model Using IFN-g Gene Knockout Donors 1

cells was greater in IFN-g gko graft recipients. Pathologic changes in IFN-g gko graft recipients were different from those typically seen in acute GVHD. The syndrome developing in IFN-g gko recipients consisted of patchy alopecia, corneal dryness and clouding, and lymphocytic infiltration of the liver, pancreas, salivary gland, lung, and kidney. Lymphocytic infiltrates were also present in the epidermis and the epithelium of both bile and salivary gland ducts. Some of the lesions closely resembled those seen in the “sicca”/Sjogren’s-like syndrome associated with chronic GVHD; however, there was no evidence of immune complex deposition in the kidney. These results indicate that GVHD in IFN-g gko graft recipients shares many features with acute GVHD, but both the duration of the disease and its pathologic manifestations are different. Our results suggest that IFN- g plays a significant role in the pathogenesis of acute GVHD by increasing the rate at which mortality develops. The Journal of Immunology, 1998, 161: 631‐ 640.