Our objective was to determine the relationship between major histocompatibility complex class I molecule expression and the tumorigenic properties of cutaneous neoplasms induced by ultraviolet radiation or chemical carcinogens. All tumors tested were found to express low constitutive levels of MHC class I molecules in vitro as determined by indirect immunofluorescence and flow cytometry. Those tumors capable of growth in UVR-exposed but not in normal recipients (regressors) were found to express enhanced levels of H-2Kk following incubation in the presence of gamma-IFN. In contrast, only one of the tumors that were capable of growth in normal recipients (progressors) exhibited more than moderate enhancement of H-2Kk expression in response to gamma-IFN. Analysis of tumor variants obtained by conversion of a UVR-induced regressor tumor to the progressor phenotype by passage through sublethally gamma-irradiated hosts, or the generation of regressor tumors by mutagen exposure of a benz [A] pyrene (BAP) induced progressor tumor, further supported the direct relationship between tumor immunogenicity in vivo and the capacity to elevate H-2Kk expression in response to gamma-IFN. No correlation existed between H-2Dk expression by the tumors and their transplantation phenotype. Furthermore, we failed to observe MHC class II expression by any of the tumors tested. Finally, the growth rate of a regressor tumor implanted into UVR-exposed hosts was significantly reduced if the tumor was pretreated with gamma-IFN in vitro prior to inoculation. This result suggests that UVR-exposed animals may be deficient in their ability to enhance the expression of MHC class I molecules on developing tumors. This alteration may, in part, account for the state of tumor susceptibility caused by UVR exposure.
We report a female patient suffering from cytomegalovirus (CMV)-induced tubulointerstitial nephritis in a renal allograft 70 days after a cadaveric renal transplantation. CMV-induced renal allograft injury reported in the literature mainly related to immune-mediated mechanisms. In our patient, acute tubulointerstitial nephritis, associated with histological evidence of CMV infection, was demonstrated in the renal allograft biopsy. There were no histological features of allograft rejection, cyclosporin nephrotoxicity nor ‘CMV glomerulopathy’. She was successfully treated by foscarnet therapy and a reduction in immunosuppression. Her renal function returned to baseline afterwards.
<i>Strongyloides stercoralis</i> infection is known to be important because of its potential for life-threatening disseminated infection in immunosuppressed hosts. Apart from direct invasion into nearly every organ in systemic infection, evidence suggests that immunological reaction also plays a role in the pathogenesis of the disease, including both uncomplicated and disseminated infections. However, Strongyloides-related glomerulonephritis has not been well documented. We present a case of steroid- and cyclophosphamide-resistant nephrotic syndrome complicated by disseminated strongyloidiasis which responded to anthelmintic agents. The remission of nephrotic syndrome after treatment of Strongyloides infection strongly suggests the possibility of Strongyloides-associated glomerulonephritis. Nephrotic patients in endemic areas of Strongyloides infection should have the differential white cell count checked. Strongyloides infection should be ruled out in patients with eosinophilia before immunosuppressants are initiated to prevent the complication of disseminated strongyloidiasis.
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