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* Lymphocyte Development Unit, Laboratory of Immunology, National Institute on Aging, National Institutes of Health, Baltimore MD 21224; and
Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, 36th and Hamilton Walk, Philadelphia, PA 19104-6082
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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1 Address correspondence and reprint requests to Dr. Jyoti M. Sen, National Institute on Aging-National Institutes of Health, 4B08 GRC Building, 5600 Nathan Shock Drive, Baltimore, MD 21224. E-mail address: Jyoti-Sen{at}nih.gov
2 Abbreviations used in this paper: BM, bone marrow; FO B, follicular B cell; MZ B, marginal zone B cell; BAFF-R, BAFF-receptor; PC, plasma cell; CSR, class-switch recombination; LEF, lymphocyte enhancer factor; TCF, T cell factor; RT, real time; ASC, Ab secreting cell; NP, 4-hydroxy-3-nitrophenylacetyl.
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