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      IL–12–Dependent, IFN–γ–Independent Experimental Glomerulonephritis

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          There is evidence that crescentic glomerulonephritis initiated in rodents by heterologous antibodies against the glomerular basement membrane (anti–GBM glomerulonephritis) depends on a Th1–type immune reaction. Interleukin 12 (IL–12) is crucial for the development of Th1 helper cells, and interferon gamma (IFN–γ) is a major proinflammatory product of these cells. In order to test the role of the two cytokines in anti–GBM glomerulonephritis we used mice lacking either the p40 chain of IL–12 (IL–12–/–) or the IFN–γ receptor (IFN–γR–/–). Glomerulonephritis was induced by injecting a rabbit anti–GBM serum in mice preimmunized against rabbit IgG. Glomerulonephritis was assessed on the basis of proteinuria, immunofluorescence findings and histology. IL–12–/– mice were completely protected against glomerulonephritis. In contrast, IFN–γR–/– mice were more severely affected than wild–type mice. Similarly, cutaneous delayed–type hypersensitivity, a typical Th1 response, was abolished in the IL–12–/–, mice but increased in the IFN–γR–/– mice. The data obtained in IL–12–/– mice support the view that crescentic glomerulonephritis in this model represents a Th1 response. Since IFN–γ is not required, other products of Th1 cells are likely to mediate glomerulonephritis.

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          Lymphocyte responses and cytokines.

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            An Interleukin (IL)-10/IL-12 Immunoregulatory Circuit Controls Susceptibility to Autoimmune Disease

            Cells of the innate immune system secrete cytokines early in immune responses that guide maturing T helper (Th) cells along appropriate lineages. This study investigates the role of cytokine networks, bridging the innate and acquired immune systems, in the pathogenesis of an organ specific autoimmune disease. Experimental allergic encephalomyelitis (EAE), a demyelinating disease of the central nervous system, is widely used as an animal model for multiple sclerosis. We demonstrate that interleukin (IL)-12 is essential for the generation of the autoreactive Th1 cells that induce EAE, both in the presence and absence of interferon γ. The disease-promoting effects of IL-12 are antagonized by IL-10 produced by an antigen nonspecific CD4+ T cell which, in turn, is regulated by the endogenous production of IL-12. This unique immunoregulatory circuit appears to play a critical role in controlling Th cell differentiation and provides a mechanism by which microbial triggers of the innate immune system can modulate autoimmune disease.
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              Imaging high-energy astrophysical sources using Earth occultation


                Author and article information

                Kidney Blood Press Res
                Kidney and Blood Pressure Research
                S. Karger AG
                24 January 2001
                : 24
                : 1
                : 27-32
                aInstitute of Anatomy, University of Zürich, Switzerland Department of Immunology, University of Cape Town, Republic of South Africa
                54202 Kidney Blood Press Res 2001;24:27–32
                © 2001 S. Karger AG, Basel

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                Page count
                Figures: 2, Tables: 2, References: 28, Pages: 6
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/54202
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