IFN-gamma receptor signaling is essential for the initiation, acceleration, and destruction of autoimmune kidney disease in MRL-Fas(lpr) mice

J Immunol. 1998 Jul 1;161(1):494-503.

Abstract

CSF-1 and TNF-alpha in the kidney of MRL-Fas(lpr) mice are proximal events that precede and promote autoimmune lupus nephritis, while apoptosis of renal parenchymal cells is a feature of advanced human lupus nephritis. In the MRL-Fas(lpr) kidney, infiltrating T cells that secrete IFN-gamma are a hallmark of disease. To examine the impact of IFN-gamma on renal injury in MRL-Fas(lpr) mice, we constructed a IFN-gamma R-deficient strain. In MRL-Fas(lpr) mice lacking IFN-gamma R, circulating and intrarenal CSF-1 were absent, TNF-alpha was markedly reduced, survival was extended, lymphadenopathy and splenomegaly were prevented, and the kidneys remained protected from destruction. Mesangial cells (MC) that were signaled through the IFN-gamma R induced CSF-1 and TNF-alpha in MRL-Fas(lpr) mice. We detected a large number of apoptotic renal parenchymal cells in advanced nephritis and determined that signaling via the IFN-gamma R induces apoptosis of tubular epithelial cells (TEC), but not MC. By comparison, TNF-alpha induces apoptosis in MC, but not TEC, of the MRL-Fas(lpr) strain. Thus, IFN-gamma is directly and indirectly responsible for apoptosis of TEC and MC in MRL-Fas(lpr) mice, respectively. In conclusion, IFN-gamma R signaling is essential for the initiation (CSF-1), acceleration (CSF-1 and TNF-alpha), and apoptotic destruction of renal parenchymal cells in MRL-Fas(lpr) autoimmune kidney disease.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Apoptosis / genetics
  • Apoptosis / immunology
  • Autoimmune Diseases / genetics
  • Autoimmune Diseases / immunology*
  • Autoimmune Diseases / mortality
  • Autoimmune Diseases / pathology*
  • Autoimmune Diseases / prevention & control
  • Cell Death
  • Down-Regulation / genetics
  • Down-Regulation / immunology
  • Epithelial Cells / immunology
  • Epithelial Cells / pathology
  • Glomerular Mesangium / metabolism
  • Glomerular Mesangium / pathology
  • Interferon gamma Receptor
  • Interferon-gamma / physiology*
  • Kidney / metabolism
  • Kidney / pathology
  • Kidney / physiopathology
  • Kidney Function Tests
  • Kidney Tubules / immunology
  • Kidney Tubules / pathology
  • Lupus Nephritis / genetics
  • Lupus Nephritis / immunology*
  • Lupus Nephritis / mortality
  • Lupus Nephritis / pathology*
  • Lupus Nephritis / prevention & control
  • Lymphatic Diseases / genetics
  • Lymphatic Diseases / immunology
  • Lymphatic Diseases / prevention & control
  • Macrophage Colony-Stimulating Factor / biosynthesis
  • Macrophage Colony-Stimulating Factor / blood
  • Macrophage Colony-Stimulating Factor / deficiency
  • Macrophage Colony-Stimulating Factor / genetics
  • Mice
  • Mice, Inbred C57BL
  • Mice, Inbred MRL lpr / genetics
  • Mice, Inbred MRL lpr / immunology*
  • Mice, Inbred Strains
  • Mice, Knockout
  • Receptors, Interferon / deficiency
  • Receptors, Interferon / genetics
  • Signal Transduction / immunology*
  • Splenomegaly / prevention & control
  • Tumor Necrosis Factor-alpha / biosynthesis
  • Tumor Necrosis Factor-alpha / metabolism
  • Tumor Necrosis Factor-alpha / pharmacology
  • fas Receptor / genetics
  • fas Receptor / immunology

Substances

  • Receptors, Interferon
  • Tumor Necrosis Factor-alpha
  • fas Receptor
  • Macrophage Colony-Stimulating Factor
  • Interferon-gamma