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Molecular and Cellular Biology, February 2007, p. 1236-1246, Vol. 27, No. 4
0270-7306/07/$08.00+0 doi:10.1128/MCB.01530-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.
Laboratory for Lymphocyte Differentiation, RIKEN Research Center for Allergy and Immunology, 1-7-22 Suehirocho, Tsurumi-ku, Yokohama, Kanagawa 230-0045, Japan,1 Department of Pathology and Pathophysiology, Osaka University Graduate School of Medicine, 2-2 Yamada-oka, Suita, Osaka 565-0871, Japan,2 Department of Biochemistry, Mie University School of Medicine, 2-174 Edobashi, Tsu, Mie 514-8507, Japan3
Received 17 August 2006/ Returned for modification 4 October 2006/ Accepted 21 November 2006
Activation of extracellular signal-regulated protein kinase (ERK) has been implicated in proliferation as well as differentiation in a wide variety of cell types. Using B-cell-specific gene-targeted mice, we report here that in T-cell-dependent immune responses, ERK2 is required to generate efficient immunoglobulin G (IgG) production. In its absence, the proportion of antigen-specific surface IgG1-bearing cells and the subsequent number of IgG1 antibody-secreting cells were decreased, despite apparently unimpaired class switch recombination. Notably, this defect was countered by overexpression of the antiapoptotic factor Bcl-2. Together, our results suggest that ERK2 plays a key role in efficient generation of antigen-specific IgG-bearing B cells by promoting their survival.
Published ahead of print on 4 December 2006.
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