Journal
JOURNAL OF IMMUNOLOGY
Volume 183, Issue 10, Pages 6831-6838Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.0900742
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Funding
- National Institutes of Health, Medimmune
- Alliance for Lupus Research
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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 anti body-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 maybe exercised at the level of the end-organ. The Journal of Immunology, 2009, 183: 6831-6838.
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