ACTIVE ANAPHYLAXIS IN IGE-DEFICIENT MICE
ACTIVE ANAPHYLAXIS IN IGE-DEFICIENT MICE
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DOI：
10.1038/370367a0
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发表时间：
1994-08-04
期刊：
影响因子：
64.8
通讯作者：
LEDER, P
中科院分区：
文献类型：
--
作者：
OETTGEN, HC;MARTIN, TR;LEDER, P
IgE触发的肥大细胞介体释放对抗原的反应被认为是速发型超敏反应（如全身性速发型过敏反应）的主要事件（1）。虽然肥大细胞和嗜碱性粒细胞可以在体外被非IgE刺激物激活（2-5），但尚不清楚这些触发物是否会导致体内生理变化。为了研究这种可能性，我们产生了CE基因纯合无效突变的小鼠。此类小鼠不产生IgE，但正常产生其他免疫球蛋白同种型。我们报告说，尽管IgE缺乏，致敏突变小鼠成为过敏性抗原的挑战，并显示心动过速和肺功能的变化类似于野生型动物。这些反应伴随着血管渗漏、血浆组胺急剧升高和快速死亡。IgE非依赖性过敏反应不依赖于补体激活，但如使用遗传免疫缺陷RAG-2（-）和SCID小鼠的研究所示，确实需要功能性免疫系统。这些结果清楚地表明，小鼠中存在超敏反应的非IgE途径。
The IgE-triggered release of mast cell mediators in response to antigen is thought to be the primary event in immediate hypersensitivity reactions such as systemic anaphylaxis(1). Although mast cells and basophils can be activated in vitro by non-IgE stimuli(2-5), it is not known whether these triggers lead to physiological changes in vivo. To investigate this possibility, we generated mice with a homozygous null mutation of the CE gene. Such mice make no IgE, but produce other immunoglobulin isotypes normally. We report that despite the IgE deficiency, sensitized mutant mice become anaphylactic on antigen challenge and display tachycardia and pulmonary function changes similar to those seen in wildtype animals. These responses are accompanied by vascular leak, sharply elevated plasma histamine and rapid death. IgE-independent anaphylaxis does not depend on complement activation, but, as indicated in studies using genetically immunodeficient RAG-2(-) and SCID mice, does require a functional immune system. Such results clearly demonstrate that non-IgE pathways for hypersensitivity reactions exist in mice.