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Role of beta-catenin in B cell development and function.
Yu, Qing; Quinn, William J; Salay, Theresa; Crowley, Jenni E; Cancro, Michael P; Sen, Jyoti Misra.
Afiliação
  • Yu Q; Lymphocyte Development Unit, Laboratory of Immunology, National Institute on Aging, National Institutes of Health, Baltimore MD 21224, USA.
J Immunol ; 181(6): 3777-83, 2008 Sep 15.
Article em En | MEDLINE | ID: mdl-18768830
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.
Assuntos

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Diferenciação Celular / Subpopulações de Linfócitos B / Beta Catenina Limite: Animals Idioma: En Ano de publicação: 2008 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Diferenciação Celular / Subpopulações de Linfócitos B / Beta Catenina Limite: Animals Idioma: En Ano de publicação: 2008 Tipo de documento: Article