Helminth parasites – masters of regulation
Identifieur interne : 000386 ( Istex/Corpus ); précédent : 000385; suivant : 000387Helminth parasites – masters of regulation
Auteurs : Rick M. Maizels ; Adam Balic ; Natalia Gomez-Escobar ; Meera Nair ; Matt D. Taylor ; Judith E. AllenSource :
- Immunological Reviews [ 0105-2896 ] ; 2004-10.
Abstract
Summary: Immune regulation by parasites is a global concept that includes suppression, diversion, and conversion of the host immune response to the benefit of the pathogen. While many microparasites escape immune attack by antigenic variation or sequestration in specialized niches, helminths appear to thrive in exposed extracellular locations, such as the lymphatics, bloodstream, or gastrointestinal tract. We review here the multiple layers of immunoregulation that have now been discovered in helminth infection and discuss both the cellular and the molecular interactions involved. Key events among the host cell population are dominance of the T‐helper 2 cell (Th2) phenotype and the selective loss of effector activity, against a background of regulatory T cells, alternatively activated macrophages, and Th2‐inducing dendritic cells. Increasingly, there is evidence of important effects on other innate cell types, particularly mast cells and eosinophils. The sum effect of these changes to host reactivity is to create an anti‐inflammatory environment, which is most favorable to parasite survival. We hypothesize therefore that parasites have evolved specific molecular strategies to induce this conducive landscape, and we review the foremost candidate immunomodulators released by helminths, including cytokine homologs, protease inhibitors, and an intriguing set of novel products implicated in immune suppression.
Url:
DOI: 10.1111/j.0105-2896.2004.00191.x
Links to Exploration step
ISTEX:159F9A40047657943A51AC6EB3CEF35DF4CABB55Le document en format XML
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While many microparasites escape immune attack by antigenic variation or sequestration in specialized niches, helminths appear to thrive in exposed extracellular locations, such as the lymphatics, bloodstream, or gastrointestinal tract. We review here the multiple layers of immunoregulation that have now been discovered in helminth infection and discuss both the cellular and the molecular interactions involved. Key events among the host cell population are dominance of the T‐helper 2 cell (Th2) phenotype and the selective loss of effector activity, against a background of regulatory T cells, alternatively activated macrophages, and Th2‐inducing dendritic cells. Increasingly, there is evidence of important effects on other innate cell types, particularly mast cells and eosinophils. The sum effect of these changes to host reactivity is to create an anti‐inflammatory environment, which is most favorable to parasite survival. We hypothesize therefore that parasites have evolved specific molecular strategies to induce this conducive landscape, and we review the foremost candidate immunomodulators released by helminths, including cytokine homologs, protease inhibitors, and an intriguing set of novel products implicated in immune suppression.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Rick M. 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Taylor</name><affiliations><json:string>Institute of Immunology and Infection Research, School of Biological Sciences, University of Edinburgh, Edinburgh, UK.</json:string></affiliations></json:item><json:item><name>Judith E. Allen</name><affiliations><json:string>Institute of Immunology and Infection Research, School of Biological Sciences, University of Edinburgh, Edinburgh, UK.</json:string></affiliations></json:item></author><articleId><json:string>IMR191</json:string></articleId><language><json:string>eng</json:string></language><originalGenre><json:string>reviewArticle</json:string></originalGenre><abstract>Summary: Immune regulation by parasites is a global concept that includes suppression, diversion, and conversion of the host immune response to the benefit of the pathogen. 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While many microparasites escape immune attack by antigenic variation or sequestration in specialized niches, helminths appear to thrive in exposed extracellular locations, such as the lymphatics, bloodstream, or gastrointestinal tract. We review here the multiple layers of immunoregulation that have now been discovered in helminth infection and discuss both the cellular and the molecular interactions involved. Key events among the host cell population are dominance of the T‐helper 2 cell (Th2) phenotype and the selective loss of effector activity, against a background of regulatory T cells, alternatively activated macrophages, and Th2‐inducing dendritic cells. Increasingly, there is evidence of important effects on other innate cell types, particularly mast cells and eosinophils. The sum effect of these changes to host reactivity is to create an anti‐inflammatory environment, which is most favorable to parasite survival. We hypothesize therefore that parasites have evolved specific molecular strategies to induce this conducive landscape, and we review the foremost candidate immunomodulators released by helminths, including cytokine homologs, protease inhibitors, and an intriguing set of novel products implicated in immune suppression.</p></abstract></profileDesc><revisionDesc><change when="2004-10">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/159F9A40047657943A51AC6EB3CEF35DF4CABB55/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Munksgaard International Publishers</publisherName><publisherLoc>Oxford, UK; Malden, USA</publisherLoc></publisherInfo><doi origin="wiley" registered="yes">10.1111/(ISSN)1600-065X</doi><issn type="print">0105-2896</issn><issn type="electronic">1600-065X</issn><idGroup><id type="product" value="IMR"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="IMMUNOLOGICAL REVIEWS">Immunological Reviews</title></titleGroup></publicationMeta><publicationMeta level="part" position="10001"><doi origin="wiley">10.1111/imr.2004.201.issue-1</doi><numberingGroup><numbering type="journalVolume" number="201">201</numbering><numbering type="journalIssue" number="1">1</numbering></numberingGroup><coverDate startDate="2004-10">October 2004</coverDate></publicationMeta><publicationMeta level="unit" type="reviewArticle" position="0008900" status="forIssue"><doi origin="wiley">10.1111/j.0105-2896.2004.00191.x</doi><idGroup><id type="unit" value="IMR191"></id></idGroup><countGroup><count type="pageTotal" number="28"></count></countGroup><titleGroup><title type="tocHeading1">Review Articles</title></titleGroup><eventGroup><event type="firstOnline" date="2004-09-10"></event><event type="publishedOnlineFinalForm" date="2004-09-10"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.2 mode:FullText source:FullText result:FullText" date="2010-03-06"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:4.0.1" date="2014-03-13"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-23"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="89">89</numbering><numbering type="pageLast" number="116">116</numbering></numberingGroup><correspondenceTo> * <i>Rick M. Maizels</i>
Institute of Immunology and Infection Research
Ashworth Laboratories, West Mains Road
University of Edinburgh, EH9 3JT, UK
Fax: +44 131 6505450
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While many microparasites escape immune attack by antigenic variation or sequestration in specialized niches, helminths appear to thrive in exposed extracellular locations, such as the lymphatics, bloodstream, or gastrointestinal tract. We review here the multiple layers of immunoregulation that have now been discovered in helminth infection and discuss both the cellular and the molecular interactions involved. Key events among the host cell population are dominance of the T‐helper 2 cell (Th2) phenotype and the selective loss of effector activity, against a background of regulatory T cells, alternatively activated macrophages, and Th2‐inducing dendritic cells. Increasingly, there is evidence of important effects on other innate cell types, particularly mast cells and eosinophils. The sum effect of these changes to host reactivity is to create an anti‐inflammatory environment, which is most favorable to parasite survival. We hypothesize therefore that parasites have evolved specific molecular strategies to induce this conducive landscape, and we review the foremost candidate immunomodulators released by helminths, including cytokine homologs, protease inhibitors, and an intriguing set of novel products implicated in immune suppression.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Helminth parasites – masters of regulation</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Maizels et al · Helminth parasites – masters of regulation</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Helminth parasites – masters of regulation</title></titleInfo><name type="personal"><namePart type="given">Rick M.</namePart><namePart type="family">Maizels</namePart><affiliation>Institute of Immunology and Infection Research, School of Biological Sciences, University of Edinburgh, Edinburgh, UK.</affiliation><affiliation>E-mail: rick.maizels@ed.ac.uk</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Adam</namePart><namePart type="family">Balic</namePart><affiliation>Institute of Immunology and Infection Research, School of Biological Sciences, University of Edinburgh, Edinburgh, UK.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Natalia</namePart><namePart type="family">Gomez‐Escobar</namePart><affiliation>Institute of Immunology and Infection Research, School of Biological Sciences, University of Edinburgh, Edinburgh, UK.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Meera</namePart><namePart type="family">Nair</namePart><affiliation>Institute of Immunology and Infection Research, School of Biological Sciences, University of Edinburgh, Edinburgh, UK.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Matt D.</namePart><namePart type="family">Taylor</namePart><affiliation>Institute of Immunology and Infection Research, School of Biological Sciences, University of Edinburgh, Edinburgh, UK.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Judith E.</namePart><namePart type="family">Allen</namePart><affiliation>Institute of Immunology and Infection Research, School of Biological Sciences, University of Edinburgh, Edinburgh, UK.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="review-article" displayLabel="reviewArticle"></genre><originInfo><publisher>Munksgaard International Publishers</publisher><place><placeTerm type="text">Oxford, UK; Malden, USA</placeTerm></place><dateIssued encoding="w3cdtf">2004-10</dateIssued><copyrightDate encoding="w3cdtf">2004</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">11</extent><extent unit="references">261</extent><extent unit="words">13629</extent></physicalDescription><abstract>Summary: Immune regulation by parasites is a global concept that includes suppression, diversion, and conversion of the host immune response to the benefit of the pathogen. While many microparasites escape immune attack by antigenic variation or sequestration in specialized niches, helminths appear to thrive in exposed extracellular locations, such as the lymphatics, bloodstream, or gastrointestinal tract. We review here the multiple layers of immunoregulation that have now been discovered in helminth infection and discuss both the cellular and the molecular interactions involved. Key events among the host cell population are dominance of the T‐helper 2 cell (Th2) phenotype and the selective loss of effector activity, against a background of regulatory T cells, alternatively activated macrophages, and Th2‐inducing dendritic cells. Increasingly, there is evidence of important effects on other innate cell types, particularly mast cells and eosinophils. The sum effect of these changes to host reactivity is to create an anti‐inflammatory environment, which is most favorable to parasite survival. 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