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J Immunol. 2009 Nov 15;183(10):6831-8. doi: 10.4049/jimmunol.0900742. Epub 2009 Oct 28.

Type I interferons produced by resident renal cells may promote end-organ disease in autoantibody-mediated glomerulonephritis.

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  • 1Department of Immunology, University of Texas Southwestern Medical Center, Dallas, TX 75390-8884, USA.

Abstract

Increased Type I IFNs or IFN-I have been associated with human systemic lupus erythematosus. Interestingly augmenting or negating IFN-I activity in murine lupus not only modulates systemic autoimmunity, but also impacts lupus nephritis, suggesting that IFN-I may be acting at the level of the end-organ. We find resident renal cells to be a dominant source of IFN-I in an experimental model of autoantibody-induced nephritis. In this model, augmenting IFN-I amplified antibody-triggered nephritis, whereas ablating IFN-I activity ameliorated disease. 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.

PMID:
19864599
[PubMed - indexed for MEDLINE]
PMCID:
PMC2876821
Free PMC Article

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