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Originally published In Press as doi:10.1074/jbc.M009242200 on December 15, 2000

J. Biol. Chem., Vol. 276, Issue 11, 8550-8556, March 16, 2001
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CD45 Is Required for CD40-induced Inhibition of DNA Synthesis and Regulation of c-Jun NH2-terminal Kinase and p38 in BAL-17 B Cells*

Yutaka ArimuraDagger §, Mami OgimotoDagger , Katsuyuki MitomoDagger , Tatsuo KatagiriDagger , Ken-ichi Yamamoto, Sinisa Volarevic||, Kazuya MizunoDagger , and Hidetaka YakuraDagger **

From the Dagger  Department of Immunology and Signal Transduction, Tokyo Metropolitan Institute for Neuroscience, Tokyo Metropolitan Organization for Medical Research, Fuchu, Tokyo 183-8526, Japan, the  Cancer Research Institute, Kanazawa University, Kanazawa 920-0934, Japan, and the || Friedrich Miecher Institute, CH-4002 Basel, Switzerland

Stimulation of B cell antigen receptor (BCR) may induce proliferation, differentiation, or apoptosis, depending upon the maturational stage of the cell and the presence or absence of signals transmitted via coreceptors. One such signal is delivered via CD40; for instance, ligation of CD40 rescues B cells from BCR-induced apoptosis. Here we show that, in contrast to WEHI-231 cells, CD40 ligation did not reverse BCR-induced growth inhibition in the BAL-17 mature B cell line and CD40 ligation itself inhibited proliferation. This inhibitory signaling was not observed in CD45-deficient cells. Further analyses demonstrate that transfection of dominant-negative form of SEK1 or treatment with SB203580 strongly reduced CD40-induced inhibition of BAL-17 proliferation, suggesting a requirement for c-Jun NH2-terminal kinase and p38 in CD40-induced inhibition of proliferation. Interestingly, CD40-initiated activation of c-Jun NH2-terminal kinase and p38 was enhanced and sustained in CD45-deficient cells, and these phenotypes were reversed by transfecting CD45 gene. However, CD40-mediated induction of cell surface molecules was not affected in CD45-deficient cells. Taken collectively, these results suggest that CD45 exerts a decisive effect on selective sets of CD40-mediated signaling pathways, dictating B cell fate.

* This work was supported in part by grants-in-aid for scientific research and for international scientific research from the Japanese Ministry of Education, Science, Sports and Culture.The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

§ Present address: Dept. of Microbiology and Immunology, Tokyo Women's Medical University, School of Medicine, Tokyo 162-8666, Japan.

** To whom correspondence should be addressed: Tokyo Metropolitan Inst. for Neuroscience, 2-6 Musashidai, Fuchu, Tokyo 183-8526, Japan. Tel.: 81-42-325-3881; Fax: 81-42-321-8678; E-mail: yakura@tmin.ac.jp.

Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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