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Blood, 7 May 2009, Vol. 113, No. 19, pp. 4566-4574.
Prepublished online as a Blood First Edition Paper on February 5, 2009; DOI 10.1182/blood-2008-08-176057.
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IMMUNOBIOLOGY
A critical role of TAK1 in B-cell receptor–mediated nuclear factor  B activation
James Schuman1,2,*,
Yuhong Chen1,*,
Andrew Podd1,2,
Mei Yu1,3,
Hong-Hsing Liu4,
Renren Wen1,
Zhijian J. Chen4,5, and
Demin Wang1,2
1 Blood Research Institute, BloodCenter of Wisconsin, Milwaukee;
2 Department of Microbiology and Molecular Genetics, Medical College of Wisconsin, Milwaukee;
3 State Key Laboratory of Pharmaceutical Biotechnology, Nanjing University, Nanjing, People's Republic of China; and
4 Department of Molecular Biology and
5 Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, Dallas
The kinase TAK1 is essential for T-cell receptor (TCR)–mediated nuclear factor  B (NF-B) activation and T-cell development. However, the role of TAK1 in B-cell receptor (BCR)–mediated NF-B 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-B after BCR stimulation. Thus, TAK1 is critical for B-cell maturation and BCR-induced NF-B activation.
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