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Mast Cells and Basophils Are Selectively Activated In Vitro and In Vivo through CD200R3 in an IgE-Independent Manner¹

Toshiyuki Kojima^*, Kazushige Obata^*, Kaori Mukai^*, Shingo Sato^*, Toshiyuki Takai, Yoshiyuki Minegishi^* and Hajime Karasuyama^2,*

^* Department of Immune Regulation, Tokyo Medical and Dental University Graduate School, Tokyo, Japan; and Department of Experimental Immunology, Institute of Development, Aging and Cancer, Tohoku University, Sendai, Japan

Mast cells and basophils have been implicated in the host defense system against pathogens and in the development of allergic disorders. Although IgE-dependent responses via FcRI on these cells have been extensively studied, little is known about cell surface molecules that are selectively expressed by these cells and engaged in their activation via an IgE-independent mechanism. We have recently established two mAbs that reacted specifically with murine mast cells and basophils, and one of them selectively depleted basophils when administered in vivo. Biochemical and flow cytometric analyses revealed that both mAbs specifically recognized a CD200R-like protein, CD200R3, but not other CD200R family members. CD200R3 existed as a disulfide-linked dimer, unlike other CD200Rs, and was expressed on mast cells and basophils primarily in association with an ITAM-bearing adaptor DAP12. Cross-linking of CD200R3 with the mAbs induced degranulation in mast cells and production of the cytokine IL-4 in basophils in vitro. Administration of the nondepleting mAb in vivo elicited systemic and local anaphylaxis in a CD200R3-dependent manner. These results suggest that CD200R3 functions as an activating receptor on mast cells and basophils to regulate IgE-independent immune responses in cooperation with an inhibitory receptor CD200R, similar to the paired receptors expressed on NK cells.

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 by Grants-in-Aid 17047013, 173709, 18659109, and 19390110 from the Japanese Ministry of Education, Culture, Sports, Science and Technology.

² Address correspondence and reprint requests to Dr. Hajime Karasuyama, Department of Immune Regulation, Tokyo Medical and Dental University Graduate School, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8519, Japan. E-mail address: karasuyama.mbch{at}tmd.ac.jp

³ Abbreviations used in this paper: BMMC, bone marrow-derived mast cells; MCMV, mouse CMV.

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