TAK1在B细胞受体介导的核因子κB激活中的关键作用。
A critical role of TAK1 in B-cell receptor-mediated nuclear factor kappaB activation.
作者信息
Schuman James, Chen Yuhong, Podd Andrew, Yu Mei, Liu Hong-Hsing, Wen Renren, Chen Zhijian J, Wang Demin
机构信息
Blood Research Institute, BloodCenter of Wisconsin, Milwaukee 53226, USA.
出版信息
Blood. 2009 May 7;113(19):4566-74. doi: 10.1182/blood-2008-08-176057. Epub 2009 Feb 5.
Abstract
The kinase TAK1 is essential for T-cell receptor (TCR)-mediated nuclear factor kappaB (NF-kappaB) activation and T-cell development. However, the role of TAK1 in B-cell receptor (BCR)-mediated NF-kappaB activation and B-cell development is not clear. Here we show that B-cell-specific deletion of TAK1 impaired the transition from transitional type 2 to mature follicular (FO) B cells and caused a marked decrease of marginal zone (MZ) B cells. TAK1-deficient B cells exhibited an increase of BCR-induced apoptosis and impaired proliferation in response to BCR ligation. Importantly, TAK1-deficient B cells failed to activate NF-kappaB after BCR stimulation. Thus, TAK1 is critical for B-cell maturation and BCR-induced NF-kappaB activation.
摘要
激酶TAK1对于T细胞受体（TCR）介导的核因子κB（NF-κB）激活和T细胞发育至关重要。然而，TAK1在B细胞受体（BCR）介导的NF-κB激活和B细胞发育中的作用尚不清楚。在此我们表明，TAK1的B细胞特异性缺失损害了从过渡2型到成熟滤泡（FO）B细胞的转变，并导致边缘区（MZ）B细胞显著减少。TAK1缺陷的B细胞表现出BCR诱导的细胞凋亡增加，并且对BCR连接的反应增殖受损。重要的是，TAK1缺陷的B细胞在BCR刺激后未能激活NF-κB。因此，TAK1对于B细胞成熟和BCR诱导的NF-κB激活至关重要。
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