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International Immunology Advance Access originally published online on July 29, 2008
International Immunology 2008 20(10):1289-1297; doi:10.1093/intimm/dxn085
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© The Japanese Society for Immunology. 2008. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

Selective impairment of Fc{varepsilon}RI-mediated allergic reaction in Gads-deficient mice

Sho Yamasaki1, Mitsuyo Takase-Utsugi2, Eri Ishikawa1, Machie Sakuma1, Keigo Nishida3, Takashi Saito1 and Osami Kanagawa2

1 Laboratory for Cell Signaling
2 Laboratory for Autoimmune Regulation
3 Laboratory for Cytokine Signaling, RIKEN Research Center for Allergy and Immunology, 1-7-22 Suehiro-cho, Tsurumi-ku, Yokohama, Kanagawa 230-0045, Japan

Correspondence to: O. Kanagawa; E-mail: kanagawa{at}rcai.riken.jp or S. Yamasaki; E-mail: sho{at}rcai.riken.jp

Gads is a Grb2-like adaptor protein expressed in hematopoietic cells. We demonstrated that mast cells from Gads–/– mice have selective functional defects. Bone marrow-derived mast cells from Gads–/– mice failed to induce Ca2+ mobilization, degranulation and cytokine production upon cross-linking of Fc{varepsilon}RI. In vivo passive cutaneous anaphylaxis was also greatly impaired in Gads–/– mice. In contrast, Gads was dispensable for Toll-like receptor-mediated cytokine production in mast cells. Accordingly, mast cell-dependent resistance to acute peritoneal bacterial infection is not reduced in Gads–/– mice in vivo. Moreover, mature T and B cell responses and antibody production upon immunization were apparently normal in Gads–/– mice. Thus, inhibition of Gads in vivo would suppress the IgE-mediated allergic reaction with minimum adverse effects on both innate and acquired immune responses, and Gads could be an ideal target for the control of allergic responses.

Keywords: Allergy, IgE, mast cells, signal transduction

Transmitting editor: K. Murphy

Received 21 March 2008, accepted 2 July 2008.


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