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J. Biol. Chem., Vol. 280, Issue 47, 38976-38981, November 25, 2005

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Critical Role of Protein Kinase C II in Activation of Mast Cells by Monomeric IgE^*

Ying Liu, Kazuyuki Furuta, Reiko Teshima, Naritoshi Shirata, Yukihiko Sugimoto, Atsushi Ichikawa¶, and Satoshi Tanaka1

From the Department of Physiological Chemistry, Graduate School of Pharmaceutical Sciences, Kyoto University, Sakyo-ku, Kyoto 606-8501, Japan, the Division of Biochemistry and Immunochemistry, National Institute of Health Sciences, Kamiyoga 1-18-1, Tokyo 158-8501, Japan, and the ^¶School of Pharmaceutical Sciences, Mukogawa Women's University, Nishinomiya, Hyogo 663-8179, Japan

Accumulating evidence suggests that IgE-mediated activation of mast cells occurs even in the absence of antigen, which is referred to as "monomeric IgE" responses. Although monomeric IgE was found to induce a wide variety of responses, such as up-regulation of the FcRI, survival, cytokine production, histamine synthesis, and adhesion to fibronectin, it remains to be clarified how mast cells are activated in the absence of antigen. It has been controversial whether monomeric IgE responses are mediated by a similar signaling mechanism to antigen stimulation, although recent studies suggest that IgE can induce the FcRI aggregation even in the absence of antigen. In this study, we focused on the role of conventional protein kinase C (cPKC), since this response is suppressed by a specific inhibitor for cPKC. Monomeric IgE-induced Ca²⁺ influx was not observed in a mouse mastocytoma cell line, which lacks the expression of PKCII, although Ca²⁺ influx induced by cross-linking of the FcRI was intact. Transfection of PKCII cDNA was found to restore the Ca²⁺ influx induced by monomeric IgE in this cell line. Furthermore, the dominant negative form of PKCII (PKCII/T500V) significantly suppressed the Ca²⁺ influx, histamine synthesis, and interleukin-6 production in another mouse mast cell line, which is highly sensitive to monomeric IgE. Expression of PKCII/T500V was found not to affect the antigen-induced responses. These results suggest that PKCII plays a critical role in monomeric IgE responses, but not in antigen responses.

Received for publication, June 10, 2005 , and in revised form, August 18, 2005.

^* This work was supported in part by grants-in-aid for Scientific Research from the Ministry of Education, Culture, Science, Sports and Technology of Japan, the Ministry of Health and Labor of Japan, and Takeda Science Foundation. 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 To whom correspondence should be addressed. Tel.: 81-75-753-4537; Fax: 81-75-753-4557; E-mail: satoshit{at}pharm.kyoto-u.ac.jp.

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