| First Author | Zheng B | Year | 2007 |
| Journal | J Immunol | Volume | 179 |
| Issue | 10 | Pages | 7087-92 |
| PubMed ID | 17982100 | Mgi Jnum | J:154008 |
| Mgi Id | MGI:4366701 | Doi | 10.4049/jimmunol.179.10.7087 |
| Citation | Zheng B, et al. (2007) Overexpression of Bcl(XL) in B cells promotes Th1 response and exacerbates collagen-induced arthritis. J Immunol 179(10):7087-92 |
| abstractText | B cells play a pathogenic or regulatory role in many autoimmune diseases through production of autoantibodies, cytokine production, and Ag presentation. However, the mechanisms that regulate these B cell functions under different autoimmune settings remain unclear. In the current study, we found that when B cells overexpress an antiapoptotic gene, Bcl(XL), they significantly increased production of IFN-gamma and enhanced Th1 response. Consistently, Bcl-x(L) transgenic mice developed more severe and sustained collagen-induced arthritis due to the enhanced Th1 response. The production of autoantibodies in Bcl(XL) transgenic mice was comparable to that in wild-type mice. Thus, our results indicate a novel role of Bcl(XL) in regulating B cell functions and immune responses. In patients with rheumatoid arthritis, arthritogenic B cells often up-regulate Bcl(XL) expression, which may not only render B cells resistant to apoptosis but also alter the ability of the autoreactive B cells to produce cytokines and modulate the inflammatory response. This may have therapeutic implications if Bcl(XL) expression can be down-regulated in autoreactive B cells. |
