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

55 Citations (Scopus)

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

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Interferon Type I
Nephritis
Glomerulonephritis
Autoantibodies
Autoimmunity
Kidney
Lupus Nephritis
Systemic Lupus Erythematosus
Monocytes
Neutrophils
Theoretical Models
Pathology
Antibodies

ASJC Scopus subject areas

  • Immunology

Cite this

Type I interferons produced by resident renal cells may promote end-organ disease in autoantibody-mediated glomerulonephritis. / Fairhurst, Anna Marie; Xie, Chun; Fu, Yuyang; Wang, Andrew; Boudreaux, Christopher; Zhou, Xin J.; Cibotti, Ricardo; Coyle, Anthony; Connolly, John E.; Wakeland, Edward K.; Mohan, Chandra.

In: Journal of Immunology, Vol. 183, No. 10, 15.11.2009, p. 6831-6838.

Research output: Contribution to journalArticle

Fairhurst, AM, Xie, C, Fu, Y, Wang, A, Boudreaux, C, Zhou, XJ, Cibotti, R, Coyle, A, Connolly, JE, Wakeland, EK & Mohan, C 2009, 'Type I interferons produced by resident renal cells may promote end-organ disease in autoantibody-mediated glomerulonephritis', Journal of Immunology, vol. 183, no. 10, pp. 6831-6838. https://doi.org/10.4049/jimmunol.0900742
Fairhurst, Anna Marie ; Xie, Chun ; Fu, Yuyang ; Wang, Andrew ; Boudreaux, Christopher ; Zhou, Xin J. ; Cibotti, Ricardo ; Coyle, Anthony ; Connolly, John E. ; Wakeland, Edward K. ; Mohan, Chandra. / Type I interferons produced by resident renal cells may promote end-organ disease in autoantibody-mediated glomerulonephritis. In: Journal of Immunology. 2009 ; Vol. 183, No. 10. pp. 6831-6838.
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AU - Fairhurst, Anna Marie

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AU - Boudreaux, Christopher

AU - Zhou, Xin J.

AU - Cibotti, Ricardo

AU - Coyle, Anthony

AU - Connolly, John E.

AU - Wakeland, Edward K.

AU - Mohan, Chandra

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AB - 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.

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