Mast cells (MCs) play a critical role in oral allergen-induced anaphylaxis. However, the contribution of basophils to the anaphylaxis remains unclear. The inhibitory immunoreceptor Allergin-1 is highly expressed on MCs and basophils and inhibits FcεRI-mediated signaling in MCs. Here, we show that Allergin-1-deficient (Milr1-/-) mice developed more severe hypothermia, a higher mortality rate and a greater incidence of diarrhea than did wild-type (WT) mice in an oral ovalbumin (OVA)-induced food allergy model. MC-deficient Mas-TRECK mice, which had been reconstituted with either WT or Milr1-/- bone marrow-derived cultured MCs, did not develop hypothermia in this food allergy model. On the other hand, depletion of basophils by injection of anti-CD200R3 antibody rescued Milr1-/- mice from lethal hypothermia but not from diarrhea. In vitro analyses demonstrated that Allergin-1 inhibits IgE-dependent activation of both human and mouse basophils. Thus, Allergin-1 on basophils selectively suppresses oral allergen-induced anaphylaxis.

中文翻译：

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Allergin-1对小鼠嗜碱性粒细胞的口服变应原诱导的过敏反应的选择性抑制。

肥大细胞（MCs）在口服过敏原引起的过敏反应中起关键作用。然而，嗜碱性粒细胞对过敏反应的贡献仍不清楚。抑制性免疫受体Allergin-1在MC和嗜碱性粒细胞上高度表达，并抑制MC中FcεRI介导的信号传导。在这里，我们显示与口服卵清蛋白（OVA）诱导的野生型（WT）小鼠相比，Allergin-1缺陷（Milr1-/-）小鼠发生了更严重的体温过低，更高的死亡率和更高的腹泻发生率食物过敏模型。MC缺陷的Mas-TRECK小鼠，已经用WT或Milr1-/-骨髓培养的MC重组，在这种食物过敏模型中没有发生体温过低的情况。另一方面，通过注射抗CD200R3抗体来消耗嗜碱性粒细胞可将Milr1-/-小鼠从致命的体温过低的情况下拯救出来，而不是从腹泻中救出。体外分析表明，Allergin-1抑制人和小鼠嗜碱性粒细胞的IgE依赖性激活。因此，嗜碱性粒细胞上的Allergin-1选择性抑制口服变应原诱导的过敏反应。