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人类类圆线虫病中L3抗原特异性抗体亚型反应:与幼虫排出量的相关性

L3 antigen-specific antibody isotype responses in human strongyloidiasis: correlations with larval output.

作者信息

Atkins N S, Conway D J, Lindo J F, Bailey J W, Bundy D A

机构信息

Centre for the Epidemiology of Infectious Disease, Department of Zoology, University of Oxford, South Parks Road, Oxford, OX1 3PS, UK.

出版信息

Parasite Immunol. 1999 Oct;21(10):517-26. doi: 10.1046/j.1365-3024.1999.00248.x.

DOI:10.1046/j.1365-3024.1999.00248.x
PMID:10587378
Abstract

Autoinfective strongyloidiasis is potentially fatal, yet the majority of infected individuals harbour asymptomatic and chronic infections. The role of humoral responses in modulating autoinfection was assessed by examining antibody isotype responses to filariform larval antigens amongst chronically infected ex-Far East Prisoners of War (exFEPOWs) with longstanding (> 30 years) infection. Serum immunoglobulin (Ig)G1, IgG4, IgE and IgA responses to whole Strongyloides stercoralis L3 extracts and their constituent antigenic components were characterized by ELISA and quantitative immunoblotting. Comparison of two groups of S. stercoralis infected exFEPOWs with and without detectable larvae in stool demonstrated novel trends. Significantly enhanced recognition of six immunodominant antigenic components by IgA was associated with undetectable larval output, as was enhanced IgE recognition of several components. Additionally, IgE and IgG4 exhibited parallel antigen recognition patterns. These findings are consistent with roles for IgA in modulating larval output, for IgE in regulating autoinfection, and for IgG4 in blocking IgE-mediated responses in human strongyloidiasis.

摘要

自身感染性类圆线虫病可能致命,但大多数感染者患有无症状的慢性感染。通过检测长期感染(超过30年)的前远东战俘(exFEPOWs)对丝状幼虫抗原的抗体同种型反应,评估了体液反应在调节自身感染中的作用。通过酶联免疫吸附测定(ELISA)和定量免疫印迹法对血清免疫球蛋白(Ig)G1、IgG4、IgE和IgA对粪类圆线虫L3提取物及其组成抗原成分的反应进行了表征。对两组粪类圆线虫感染的exFEPOWs(一组粪便中可检测到幼虫,另一组未检测到)的比较显示出新的趋势。IgA对六种免疫显性抗原成分的显著增强识别与未检测到幼虫排出相关,IgE对几种成分的增强识别也是如此。此外,IgE和IgG4表现出平行的抗原识别模式。这些发现与IgA在调节幼虫排出、IgE在调节自身感染以及IgG4在阻断人体类圆线虫病中IgE介导的反应中的作用一致。

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