Type I interferons produced by resident renal cells may promote end-organ disease in autoantibody-mediated glomerulonephritis.
Type I interferons produced by resident renal cells may promote end-organ disease in autoantibody-mediated glomerulonephritis.
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DOI：
10.4049/jimmunol.0900742
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发表时间：
2009-11-15
期刊：
影响因子：
--
通讯作者：
Mohan C
中科院分区：
文献类型：
--
作者：
Fairhurst AM;Xie C;Fu Y;Wang A;Boudreaux C;Zhou XJ;Cibotti R;Coyle A;Connolly JE;Wakeland EK;Mohan C
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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影响因子：
13.6
作者：
de Lema, GP;Maier, H;Luckow, B
通讯作者：
Luckow, B
影响因子：
5.4
作者：
Allam, Ramanjaneyulu;Pawar, Rahul D.;Anders, Hans-Joachim
通讯作者：
Anders, Hans-Joachim
全身IFN-α在B6.SLE123小鼠中驱动肾脏肾炎。
影响因子：
5.4
作者：
Fairhurst, Anna-Marie;Mathian, Alexis;Connolly, John E.;Wang, Andrew;Gray, Hillery F.;George, Tiffany A.;Boudreaux, Christopher D.;Zhou, Xin J.;Li, Quan-Zhen;Koutouzov, Sophie;Banchereau, Jacques;Wakeland, Edward K.
通讯作者：
Wakeland, Edward K.
DOI：
10.1084/jem.20021553
发表时间：
2003-03-17
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Bennett L;Palucka AK;Arce E;Cantrell V;Borvak J;Banchereau J;Pascual V
通讯作者：
Pascual V
影响因子：
4.4
作者：
Fu, YY;Xie, C;Mohan, C
通讯作者：
Mohan, C