Regulatory B cells (B10 cells) have a suppressive role in murine lupus: CD19 and B10 cell deficiency exacerbates systemic autoimmunity.
Regulatory B cells (B10 cells) have a suppressive role in murine lupus: CD19 and B10 cell deficiency exacerbates systemic autoimmunity.
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DOI：
10.4049/jimmunol.0902385
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发表时间：
2010-05-01
期刊：
影响因子：
--
通讯作者：
Fujimoto M
中科院分区：
文献类型：
--
作者：
Watanabe R;Ishiura N;Nakashima H;Kuwano Y;Okochi H;Tamaki K;Sato S;Tedder TF;Fujimoto M
B cells play critical roles in the pathogenesis of lupus. To examine the influence of B cells on disease pathogenesis in a murine lupus model, New Zealand Black and New Zealand White F1 hybrid (NZB/W) mice were generated that were deficient for CD19 (CD19−/− NZB/W mice), a B cell-specific cell surface molecule that is essential for optimal B cell signal transduction. The emergence of anti-nuclear antibodies was significantly delayed in CD19−/− NZB/W mice in comparison with wild type NZB/W mice. However, the pathologic manifestations of nephritis appeared significantly earlier and survival was significantly reduced in CD19−/− NZB/W mice in comparison with wild type mice. These results demonstrate both disease promoting and protective roles for B cells in lupus pathogenesis. Recent studies have identified a potent regulatory B cell subset (B10 cells) within the rare CD1dhiCD5+ B cell subset of the spleen that regulates acute inflammation and autoimmunity through the production of IL-10. In wild type NZB/W mice, the CD1dhiCD5+B220+ B cell subset that includes B10 cells was increased by 2.5-fold during the disease course, while CD19−/− NZB/W mice lacked this CD1dhiCD5+ regulatory B cell subset. However, the transfer of splenic CD1dhiCD5+ B cells from wild type NZB/W mice into CD19−/− NZB/W recipients significantly prolonged their survival. Furthermore, regulatory T cells were significantly decreased in CD19−/− NZB/W mice, but the transfer of wild type CD1dhiCD5+ B cells induced Treg cell expansion in CD19−/− NZB/W mice. These results demonstrate an important protective role for regulatory B10 cells in this systemic autoimmune disease.
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影响因子：
9.1
作者：
Chun, Hye-Young;Chung, Jae-Wook;Suh, Chang-Hee
通讯作者：
Suh, Chang-Hee
影响因子：
4.4
作者：
Fujimoto, M;Poe, JC;Tedder, TF
通讯作者：
Tedder, TF
Toll样受体9控制鼠狼疮中的抗DNA自身抗体产生。
DOI：
10.1084/jem.20050338
发表时间：
2005-07-18
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Christensen SR;Kashgarian M;Alexopoulou L;Flavell RA;Akira S;Shlomchik MJ
通讯作者：
Shlomchik MJ
DOI：
10.1084/jem.189.10.1639
发表时间：
1999-05-17
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Chan OT;Hannum LG;Haberman AM;Madaio MP;Shlomchik MJ
通讯作者：
Shlomchik MJ
影响因子：
12.8
作者：
Gonzalez-Amaro, R;Portales-Perez, D;Alaron-Segovia, D
通讯作者：
Alaron-Segovia, D