| First Author | Yu Q | Year | 2008 |
| Journal | J Immunol | Volume | 181 |
| Issue | 6 | Pages | 3777-83 |
| PubMed ID | 18768830 | Mgi Jnum | J:139115 |
| Mgi Id | MGI:3807337 | Doi | 10.4049/jimmunol.181.6.3777 |
| Citation | Yu Q, et al. (2008) Role of beta-catenin in B cell development and function. J Immunol 181(6):3777-83 |
| abstractText | beta-Catenin is a central mediator of Wnt signaling pathway, components of which have been implicated in B cell development and function. B cell progenitors and bone marrow stromal cells express Wnt ligands, Frizzled receptors and Wnt antagonists, suggesting fine tuned regulation of this pathway in B cell development. In particular, deletion of Frizzled 9 gene results in developmental defects at the pre-B stage of development and an accumulation of plasma cells. Furthermore, Wnt signals regulate B cell proliferation through lymphocyte enhancer-binding factor-1. However, it is not known whether Wnt signaling in B cell development is mediated by beta-catenin and whether beta-catenin plays a role in mature B cell function. In this report, we show that mice bearing B cell-specific deletion of beta-catenin have normal B cell development in bone marrow and periphery. A modest defect in plasma cell generation in vitro was documented, which correlated with a defective expression of IRF-4 and Blimp-1. However, B cell response to T-dependent and T-independent Ags in vivo was found to be normal. Thus, beta-catenin expression was found to be dispensable for normal B cell development and function. |
