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See Latest ArticlesType I Interferons Produced by Resident Renal Cells May Promote End-Organ Disease in Autoantibody-Mediated Glomerulonephritis
Journal of Immunology, 11/09/09
Fairhurst AM et al. – One mechanism through which increased IFN–I drives immune–mediated nephritis might be operative through increased recruitment of inflammatory monocytes and neutrophils, though this hypothesis needs further validation. Collectively, these studies indicate that an important contribution of IFN–I toward the disease pathology seen in systemic autoimmunity may be exercised at the level of the end–organ.
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