Abstract
Little is known about the potential role of T cells in the inflammatory renal disease glomerulonephritis (GN). GN has been historically viewed as a product of immune complex-mediated complement activation, and the presence of autoantibodies made identifying T cell-specific effector contributions difficult to elucidate. In this issue of the JCI, Heymann et al. generate what they believe to be a novel, transgenic murine model of GN, demonstrating a direct role for CD8+ T cells, activated CD4+ T cells, and DCs in the pathogenesis of GN (see the related article beginning on page 1286).
MeSH terms
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Animals
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Antigen Presentation / immunology
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Autoimmune Diseases / etiology
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Autoimmune Diseases / immunology
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Autoimmune Diseases / pathology
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CD4-Positive T-Lymphocytes / immunology
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CD4-Positive T-Lymphocytes / transplantation
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CD8-Positive T-Lymphocytes / immunology
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CD8-Positive T-Lymphocytes / transplantation
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Dendritic Cells / immunology*
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Disease Models, Animal*
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Glomerulonephritis / immunology*
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Glomerulonephritis / pathology*
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Kidney / immunology
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Kidney / pathology
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Lymph Nodes / immunology
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Lymphocyte Activation / immunology
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Mice
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Mice, Transgenic
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Ovalbumin / genetics
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Ovalbumin / immunology
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Podocytes / metabolism
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T-Lymphocytes / immunology*
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T-Lymphocytes / transplantation