Abstract
β-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 β-catenin and whether β-catenin plays a role in mature B cell function. In this report, we show that mice bearing B cell-specific deletion of β-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, β-catenin expression was found to be dispensable for normal B cell development and function.
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CITATION STYLE
Yu, Q., Quinn, W. J., Salay, T., Crowley, J. E., Cancro, M. P., & Sen, J. M. (2008). Role of β-Catenin in B Cell Development and Function. The Journal of Immunology, 181(6), 3777–3783. https://doi.org/10.4049/jimmunol.181.6.3777
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