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Fcγ 受体抑制小鼠和人嗜碱性粒细胞的活化。

Fcγ receptors inhibit mouse and human basophil activation.

机构信息

Unité d'Allergologie Moléculaire et Cellulaire, Département d'Immunologie, Institut Pasteur, 75015 Paris, France.

出版信息

J Immunol. 2012 Sep 15;189(6):2995-3006. doi: 10.4049/jimmunol.1200968. Epub 2012 Aug 20.

Abstract

Besides high-affinity IgE receptors (FcεRI), human basophils express activating (FcγRIIA) and inhibitory (FcγRIIB) low-affinity IgG receptors. IgG receptors (FcγR) were also found on mouse basophils, but not identified. We investigated in this study FcγR and the biological consequences of their engagement in basophils of the two species. We found the following: (1) that mouse basophils also express activating (FcγRIIIA) and inhibitory (FcγRIIB) low-affinity FcγR; (2) that activating FcγR can activate both human and mouse basophils, albeit with different efficacies; (3) that negative signals triggered by inhibitory FcγR are dominant over positive signals triggered by activating FcγR, thus preventing both human and mouse basophils from being activated by IgG immune complexes; (4) that the coengagement of FcεRI with inhibitory and activating FcγR results in a FcγRIIB-dependent inhibition of IgE-induced responses of both human and mouse basophils; (5) that FcγRIIB has a similar dominant inhibitory effect in basophils from virtually all normal donors; and (6) that IL-3 upregulates the expression of both activating and inhibitory FcγR on human basophils from normal donors, but further enhances FcγRIIB-dependent inhibition. FcγR therefore function as a regulatory module, made of two subunits with antagonistic properties, that prevents IgG-induced and controls IgE-induced basophil activation in both mice and humans.

摘要

除了高亲和力 IgE 受体 (FcεRI),人类嗜碱性粒细胞还表达激活型 (FcγRIIA) 和抑制型 (FcγRIIB) 低亲和力 IgG 受体。FcγR 也存在于小鼠嗜碱性粒细胞上,但尚未鉴定。在本研究中,我们研究了这两种物种的嗜碱性粒细胞中 FcγR 的表达及其激活的生物学后果。我们发现:(1) 小鼠嗜碱性粒细胞也表达激活型 (FcγRIIIA) 和抑制型 (FcγRIIB) 低亲和力 FcγR;(2) 激活型 FcγR 可以激活人和小鼠的嗜碱性粒细胞,尽管效率不同;(3) 抑制型 FcγR 触发的负信号占优势,超过激活型 FcγR 触发的正信号,从而防止 IgG 免疫复合物激活人和小鼠的嗜碱性粒细胞;(4) FcεRI 与抑制型和激活型 FcγR 的共结合导致 FcγRIIB 依赖性抑制人源和鼠源嗜碱性粒细胞的 IgE 诱导反应;(5) FcγRIIB 在几乎所有正常供体的嗜碱性粒细胞中具有相似的主要抑制作用;(6) IL-3 上调正常供体人嗜碱性粒细胞上激活型和抑制型 FcγR 的表达,但进一步增强了 FcγRIIB 依赖性抑制。FcγR 因此作为一个调节模块发挥作用,由具有拮抗特性的两个亚基组成,可防止 IgG 诱导的和控制 IgE 诱导的人和小鼠嗜碱性粒细胞的激活。

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