An immunoglobulin-like receptor, Allergin-1, inhibits immunoglobulin E-mediated immediate hypersensitivity reactions

被引:57
作者
Hitomi, Kaori [1 ]
Tahara-Hanaoka, Satoko [1 ]
Someya, Satoru [1 ]
Fujiki, Akira [2 ]
Tada, Hideaki [2 ]
Sugiyama, Tetsuya [2 ]
Shibayama, Shiro [2 ]
Shibuya, Kazuko [1 ]
Shibuya, Akira [1 ]
机构
[1] Univ Tsukuba, Inst Basic Med Sci, Dept Immunol, Grad Sch Comprehens Human Sci, Tsukuba, Ibaraki 305, Japan
[2] Tsukuba Res Inst, Exploratory Res Labs, Tsukuba, Ibaraki, Japan
关键词
MAST-CELL ACTIVATION; FC-EPSILON-RI; SYSTEMIC-ANAPHYLAXIS; NEGATIVE REGULATION; BASOPHILS PLAY; GAMMA RIII; IGE; IDENTIFICATION; DEGRANULATION; MOTIFS;
D O I
10.1038/ni.1886
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Anaphylaxis is a life-threatening immediate hypersensitivity reaction triggered by antigen capture by immunoglobulin E (IgE) bound to the high-affinity IgE receptor (Fc epsilon RI) on mast cells. However, the regulatory mechanism of mast cell activation is not completely understood. Here we identify an immunoglobulin-like receptor, Allergin-1, that contains an immunoreceptor tyrosine-based inhibitory motif (ITIM)-like domain, and show it was preferentially expressed on mast cells. Mouse Allergin-1 recruited the tyrosine phosphatases SHP-1 and SHP-2 and the inositol phosphatase SHIP. Coligation of Allergin-1 and FceRI suppressed IgE-mediated degranulation of bone marrow-derived cultured mast cells. Moreover, mice deficient in Allergin-1 developed enhanced passive systemic and cutaneous anaphylaxis. Thus, Allergin-1 suppresses IgE-mediated, mast cell-dependent anaphylaxis in mice.
引用
收藏
页码:601 / U61
页数:8
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