REGULATION OF MHC EXPRESSION INVIVO .2. IFN-ALPHA-BETA INDUCERS AND RECOMBINANT IFN-ALPHA MODULATE MHC ANTIGEN EXPRESSION IN MOUSE-TISSUES

  • 15 June 1989
    • journal article
    • research article
    • Vol. 142  (12) , 4241-4247
Abstract
We examined the effect of type I IFN inducers and rIFN-.alpha. on MHC expression in mouse tisues in vivo. MHC expression was assessed in a radiolabeled mAb binding assay and by indirect immunoperoxidase staining of tissue sections. polyI:C, an inducer of IFN-.alpha./.beta., induced large increases in class I MHC in many tissues, with little effect on class II expression. In the kidney, which was studied in detail, polyI:C increased class I expression from day 1 to day 6, localized in glomeruli, tubules, and arterial endothelium. Renal class II MHC was less affected but tended to be decreased at days 3 to 6, corresponding to diminished staining of class II-positive interstitial cells. polyI:C increased renal class I MHC in nude mice andmice with severe combined immunodeficiency, and in mice treated with cyclosporine or mAb against IFN-.gamma.. The effects of influenza virus resembled those of polyI:C. However, a potent T cell stimulus, allogeneic ascites tumor cells, induced markedly different MHC changes, with massive and sustained increases in class I and II, presumably due to IFN-.gamma. release, which was inhibited by cyclosporine or by mAb against IFN-.gamma.. The effect of polyI:C was largely simulated by rIFN-.gamma.. Thus, rIFN-.alpha. and its inducers in vivo produce a sustained increase in renal class I expression in kidney and other tissues, sometimes with changes in class II expression. Such effects could be relevant to the immune modulatory actions of IFN, and to the immunologic consequences of viral infections.