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Regulation of cell surface FcεRI expression by IgE. Implication in allergy

IgE 调节细胞表面 FcεRI 表达对过敏的影响。

基本信息

批准号：
10670409
负责人：
NAKAJIMA Toshiharu
金额：
$ 1.92万
依托单位：
The University of Tokyo
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1998
资助国家：
日本
起止时间：
1998 至 1999
项目状态：
已结题

项目摘要

We investigated whether IL-4 and IgE regulate surface expression and function of FcεRI in eosinophils, as with mast cells. Eosinophils were purified from venous blood from consenting volunteers with no history of atopic diseases. Cells were cultured with IL-5, and with or without IL-4 and/or IgE at 37℃. After culture for 7 days, the surface FcεRI expression on eosinophils was analyzed by flow cytometry using anti-FcεRI mAb, CRA-1. Although peripheral blood eosinophils did not express surface FcεRI, apparent FcεRI expression (up to 1% of mast cell FcεRI levels) was observed in eosinophils cultured with both IL-4 and IgE from all donors. The combination of IL-4 and IgB was necessary for the maximal induction of surface FcεRI expression. In the presence of IL-4 and IgE, eosinophils cultured for 2 days demonstrated low but statistically significant levels of surface FcεRI, which reached to plateau after 7 days of culture. However, cross-linking of surface FcεRI by CRA-1 failed to induce the release of eosiaophil-derived neurotoxin (EDN) or leukotriene (LT) C4, or CaィイD12+ィエD1 influx in eosinophils cultured for 7 days with IL-4 and IgE. These results suggest that surface FcεRI expression in eosinophils is regulated by a mechanism similar to that in mast cells.

我们研究了IL-4和IgE是否调节嗜酸性粒细胞中FcεRI的表面表达和功能，就像肥大细胞一样。从无过敏性疾病史的自愿者的静脉血中纯化嗜酸性粒细胞。在37℃下，用IL-5、IL-4和/或IgE培养细胞。培养7天后，使用抗Fc εRI mAb CRA-1通过流式细胞术分析嗜酸性粒细胞表面FcεRI表达。虽然外周血嗜酸性粒细胞不表达表面FcεRI，但在所有供体的IL-4和IgE培养的嗜酸性粒细胞中观察到明显的FcεRI表达（高达肥大细胞FcεRI水平的1%）。IL-4和IgB的组合是最大程度地诱导表面FcεRI表达所必需的。在IL-4和IgE的存在下，培养2天的嗜酸性粒细胞表现出低但具有统计学意义的表面FcεRI水平，其在培养7天后达到平台期。然而，CRA-1交联表面FcεRI不能诱导嗜酸性粒细胞释放嗜酸性粒细胞衍生的神经毒素（EDN）或白三烯（LT）C4，也不能诱导与IL-4和IgE共同培养7天的嗜酸性粒细胞中Ca ~（2+）D12+ Ca ~（2+）D1内流。这些结果表明，嗜酸性粒细胞表面FcεRI的表达受与肥大细胞相似的机制调控。