期刊
JOURNAL OF IMMUNOLOGY
卷 184, 期 5, 页码 2289-2296出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.0903133
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资金
- American College of Rheumatology Research and Education Foundation
- Alliance for Lupus Research Target Identification in Lupus program
- Veterans Administration Merit Review [1I01BX000600-01]
- Daiichi-Sankyo
- National Institutes of Health [1AI 071110-01A1, ARRA 3RO1A171110-02S1, RR-020136, AI 083539Z]
- Arthritis Foundation
- Lupus Research Institute
- [DK 064400]
We previously identified that autoreactive B cells from BXD2 mice can be targeted by 11,47, leading to upregulation of the expression of regulators of G-protein signaling (Rgs) genes that facilitated the development of spontaneous germinal centers. Little is known about the signaling pathway used by IL-17 to upregulate RGS. In the current study, we found that IL-17 rapidly activates the canonical NF-kappa B signaling pathway and that BXD2 B cells exhibit higher basal and activated phosphorylated p65 levels than B6 or BXD2-Il17ra(-/-) B cells. Inhibition of p65 phosphorylation downregulated RGS16 expression and abrogated the IL-17-induced chemotactic arrest of B cells in response to CXCL12. Knockdown of TNFR-associated factor 6 or NF-kappa B activator I in 70Z/3 pre-B cells led to decreased Rgs,16 expression, indicating that both of these two genes are involved in IL-17-mediated activation of NF-kappa B signaling in B cells. These findings identify the signaling pathway regulated by IL-17 to contribute to the development of spontaneous germinal centers in autoimmune BXD2 mice. The Journal of Immunology, 2010, 184: 2289-2296.
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