Suppr超能文献

烟曲霉过敏原I是一种主要的IgE结合蛋白,属于细胞毒素米托吉林家族的成员。

Aspergillus fumigatus allergen I, a major IgE-binding protein, is a member of the mitogillin family of cytotoxins.

作者信息

Arruda L K, Platts-Mills T A, Fox J W, Chapman M D

机构信息

Department of Internal Medicine, University of Virginia, Charlottesville 22908.

出版信息

J Exp Med. 1990 Nov 1;172(5):1529-32. doi: 10.1084/jem.172.5.1529.

Abstract

A major 18-kD IgE-binding protein from Aspergillus fumigatus (Asp fI) has been purified. Partial amino acid sequencing of Asp f I showed extensive sequence homology (95%) between Asp fI and a cytotoxin (mitogillin) produced by A. restrictus. Crossinhibition radioimmunoassay using murine monoclonal antibody and human IgG and IgE antibodies showed that Asp fI and mitogillin were antigenically indistinguishable. Furthermore, both proteins inhibited protein synthesis in vitro by greater than 90%. Asp fI was expressed in A. fumigatus but not in seven other Aspergillus species. The results suggest that Asp fI could play a dual role in the pathogenesis of A. fumigatus-related diseases by promoting colonization through cytotoxic activity and by causing inflammatory reactions involving IgE antibodies.

摘要

来自烟曲霉的一种主要的18-kD IgE结合蛋白(Asp fI)已被纯化。Asp fI的部分氨基酸序列分析表明,Asp fI与局限曲霉产生的一种细胞毒素(丝裂毒素)之间存在广泛的序列同源性(95%)。使用鼠单克隆抗体以及人IgG和IgE抗体进行的交叉抑制放射免疫测定表明,Asp fI和丝裂毒素在抗原性上无法区分。此外,这两种蛋白在体外均能抑制超过90%的蛋白质合成。Asp fI在烟曲霉中表达,但在其他七种曲霉属物种中不表达。结果表明,Asp fI可能在烟曲霉相关疾病的发病机制中发挥双重作用,即通过细胞毒性活性促进定植,并通过引发涉及IgE抗体的炎症反应。

相似文献

引用本文的文献

4
Fumagillin Contributes to Host Cell Damage.烟曲霉素会导致宿主细胞损伤。
J Fungi (Basel). 2021 Nov 3;7(11):936. doi: 10.3390/jof7110936.

本文引用的文献

7
A pathologic study of allergic bronchopulmonary aspergillosis.
J Allergy Clin Immunol. 1988 Apr;81(4):718-25. doi: 10.1016/0091-6749(88)91044-5.
10
Aspergillus, asthma, and amoebae.
Lancet. 1989 Apr 22;1(8643):893-4. doi: 10.1016/s0140-6736(89)92877-8.

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验