Journal
BLOOD
Volume 113, Issue 19, Pages 4566-4574Publisher
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2008-08-176057
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Funding
- National Institutes of Health [R01 AI52327, RO1 AI60919, R01 AI079087, R01 HL073284]
- Leukemia & Lymphoma Society
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The kinase TAK1 is essential for T-cell receptor (TCR)-mediated nuclear factor kappa B (NF-kappa B) activation and T-cell development. However, the role of TAK1 in B-cell receptor (BCR)-mediated NF-kappa 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-kappa B after BCR stimulation. Thus, TAK1 is critical for B-cell maturation and BCR-induced NF-kappa B activation. (Blood. 2009;113:4566-4574)
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