International Immunology, Vol. 11, No. 2, 199-207,
February 1999
© 1999 Japanese Society for Immunology
Fc receptor ß subunit is required for full activation of mast cells through Fc receptor engagement
Department of Immunology, Juntendo University School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo 113-8421, Japan
1 Division of Molecular Immunology, Center for Biomedical Science, School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-Ku, Chiba-City 260, Japan
2 Department of Immunolgy, Mitubishi Kasei Institute of Life Sciences 11 Minami-ooya Machida-City, Tokyo 194, Japan
Correspondence to: C. Ra
The high-affinity IgE receptor (Fc
RI) and the low-affinity IgG receptor (Fc
RIII) on mast cells are the key molecules involved in triggering the allergic reaction. These receptors share the common ß subunit (FcRß) which contains an immunoreceptor tyrosine-based activation motif and transduces the signals of these receptors' aggregation. In rodents, FcRß is essential for the cell surface expression of the FcRI. In humans, the FcRß gene was reported to be one of the candidate genes causing atopic diseases. However, the role of FcRß in vivo still remains ambiguous. To elucidate the functions of FcRß, we developed the mice lacking FcRß [FcRß(–/–)]. The FcRß(–/–) mice lacked the expression of the FcRI on mast cells and IgE-mediated passive cutaneous anaphylaxis (PCA) was not induced in FcRß(–/–) mice as was expected. In these mice, the expression of IgG receptors on mast cells was augmented but the IgG-mediated PCA reaction was attenuated. Although with bone marrow-derived cultured mast cells from FcRß(–/–), adhesion to fibronectin and Ca2+ flux upon aggregation of IgG receptors were enhanced, mast cells co-cultured with 3T3 fibroblasts exhibited impaired degranulation on receptor aggregation. These observations indicate that FcRß accelerates the degranulation of mature mast cells via the IgG receptor in connective tissues.
Keywords: FcRß knock-out mouse, Fc
RI, FcR, immunoreceptor tyrosine-based activation motif, mast cell
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