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      Blockade of IL-18 receptor signaling delays the onset of autoimmune disease in MRL-Faslpr mice.

      The Journal of Immunology Author Choice

      pathology, Antigens, CD95, genetics, Autoimmune Diseases, etiology, prevention & control, Blood Urea Nitrogen, Cytokines, Hypergammaglobulinemia, Interferon-gamma, physiology, Interleukin-18 Receptor alpha Subunit, Kidney, Animals, Lung, Lymphatic Diseases, Mice, Mice, Inbred MRL lpr, Proteinuria, RNA, Messenger, analysis, Receptors, Interleukin, antagonists & inhibitors, Receptors, Interleukin-18, Signal Transduction, Skin

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          Abstract

          Autoimmune disease in Fas-deficient MRL-Faslpr mice is dependent on infiltrating autoreactive leukocytes and autoantibodies, and IFN-gamma plays an important role in the pathogenesis. As IL-18 is capable of inducing IFN-gamma production in T cells, we hypothesized that signaling through IL-18R is involved in the pathogenesis. To investigate the impact of IL-18 in this autoimmune disease, we generated an MRL-Faslpr strain deficient in IL-18Ralpha. Compared with the wild-type strain, IL-18Ralpha-deficient MRL-Faslpr mice survived longer and showed a significant reduction in renal pathology, including glomerular IgG deposits, proteinuria, and serum anti-DNA Abs. Intrarenal transcripts encoding IFN-gamma, TNF-alpha, IL-12, and IL-10, which have been linked to nephritis, were all markedly reduced. Skin lesions, lymphadenopathy, and lung pathology characteristic of the MRL-Faslpr mouse disease were diminished in IL-18Ralpha-deficient MRL-Faslpr mice. Thus, we conclude that IL-18Ralpha signaling is critical to the pathogenesis of autoimmune disease in MRL-Faslpr mice.

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