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

Anna Marie Fairhurst, Chun Xie, Yuyang Fu, Andrew Wang, Christopher Boudreaux, Xin J. Zhou, Ricardo Cibotti, Anthony Coyle, John E. Connolly, Edward K. Wakeland, Chandra Mohan

Research output: Contribution to journalArticle

58 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)6831-6838
Number of pages8
JournalJournal of Immunology
Volume183
Issue number10
DOIs
StatePublished - Nov 15 2009

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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    Fairhurst, A. M., Xie, C., Fu, Y., Wang, A., Boudreaux, C., Zhou, X. J., Cibotti, R., Coyle, A., Connolly, J. E., Wakeland, E. K., & Mohan, C. (2009). Type I interferons produced by resident renal cells may promote end-organ disease in autoantibody-mediated glomerulonephritis. Journal of Immunology, 183(10), 6831-6838. https://doi.org/10.4049/jimmunol.0900742