A critical role of TAK1 in B-cell receptor-mediated nuclear factor kappaB activation

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.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis / physiology
  • B-Lymphocytes / metabolism*
  • Blotting, Western
  • Cell Nucleus / metabolism
  • Electrophoretic Mobility Shift Assay
  • Flow Cytometry
  • Fluorescent Antibody Technique
  • MAP Kinase Kinase Kinases / physiology*
  • Mice
  • Mice, Knockout
  • NF-kappa B / metabolism*
  • Receptors, Antigen, B-Cell / metabolism*
  • Signal Transduction

Substances

  • NF-kappa B
  • Receptors, Antigen, B-Cell
  • MAP Kinase Kinase Kinases
  • MAP kinase kinase kinase 7