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Augmentation of Signaling through BCR Containing IgE but not That Containing IgA Due to Lack of CD22-Mediated Signal Regulation¹

Motohiko Sato^*,, Takahiro Adachi^*,, and Takeshi Tsubata^2,*,,

^* Laboratory of Immunology, School of Biomedical Science, and Department of Immunology, Medical Research Institute, Tokyo Medical and Dental University, Tokyo, Japan; and Core Research for Engineering, Science, and Technology, Japan Science and Technology, Tokyo, Japan

The B cell membrane molecules CD22 and CD72 contain ITIMs in their cytoplasmic portion, and negatively regulate signaling through BCR. Various lines of evidence suggest that ligation of BCR containing IgG (IgG-BCR) transmits augmented signaling due to lack of CD22-mediated signal regulation. However, the signaling capacities of BCR containing IgA and IgE remain largely undefined. In this study, we demonstrate that both IgE-BCR and IgG-BCR, but not IgA-BCR, transmit augmented signaling compared with IgM-BCR. Ligation of IgE-BCR does not induce signaling events required for CD22-mediated signal inhibition, and restoration of these signaling events by coligation of CD22 with BCR abrogates signal augmentation. Furthermore, the cytoplasmic portion of IgE but not that of IgA is sufficient for suppressing CD22-mediated signal inhibition. These findings strongly suggest that the cytoplasmic portion of IgE but not that of IgA reverses CD22-mediated signal inhibition, leading to augmentation of signaling through IgE-BCR but not IgA-BCR. Augmented IgE-BCR signaling appears to play a role in production of large amounts of IgE during helminth infection, whereas regulated signaling through IgA-BCR may be crucial for constitutive production of IgA for mucosal immunity.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported in part by grants from the Ministry of Education, Culture, Sports, Science and Technology of Japan, Japan Society for the Promotion of Science, and the Ichiro Kanehara Foundation.

² Address correspondence and reprint requests to Dr. Takeshi Tsubata, Laboratory of Immunology, School of Biomedical Science, and Department of Immunology, Medical Research Institute, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8510, Japan. E-mail address: tsubata.imm{at}mri.tmd.ac.jp

³ Abbreviations used in this paper: SHP-1, Src homology 2 domain-containing protein tyrosine phosphatase-1; NP, (4-hydroxy-3-nitrophenyl) acetyl.

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