The Journal of Experimental Medicine
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© The Rockefeller University Press, 0022-1007/1998/4/1343/ $5.00
The Journal of Experimental Medicine, Volume 187, Number 8, April 20, 1998 1343-1348

Brief Definitive Reports

A Double-Edged Kinase Lyn: A Positive and Negative Regulator for Antigen Receptor–mediated Signals

Hirofumi Nishizumi*,{ddagger}, Keisuke Horikawa*, Irena Mlinaric-Rascan*, and Tadashi Yamamoto*

From the * Department of Oncology, Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan; and the {ddagger} Department of Biophysics and Biochemistry, Graduate School of Science, The University of Tokyo, Tokyo 113-0033, Japan

B cells from young lyn–/– mice are hyperresponsive to anti-IgM–induced proliferation, suggesting involvement of Lyn in negative regulation of B cell antigen receptor (BCR)-mediated signaling. Here we show that tyrosine phosphorylation of Fc{gamma}RIIB and CD22 coreceptors, which are important for feedback suppression of BCR-induced signaling, was severely impaired in lyn–/– B cells upon their coligation with the BCR. Hypophosphorylation on tyrosine residues of these molecules resulted in failure of recruiting the tyrosine phosphatase SHP-1 and inositol phosphatase SHIP, SH2-containing potent inhibitors of BCR-induced B cell activation, to the coreceptors. Consequently, lyn–/– B cells exhibited defects in suppressing BCR-induced Ca2+ influx and proliferation. Thus, Lyn is critically important in tyrosine phosphorylation of the coreceptors, which is required for feedback suppression of B cell activation.

Address correspondence to Tadashi Yamamoto, Department of Oncology, Institute of Medical Science, The University of Tokyo, Shirokanedai 4-6-1, Minato-ku, Tokyo 108-8639, Japan. Phone: 81-3-5449-5301; Fax: 81-3-5449-5413; E-mail: tyamamot{at}ims.u-tokyo.ac.jp


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