IL-27 promotes IL-10 production by effector Th1 CD4+ T cells; a critical mechanism for protection from severe immunopathology during malaria infection1
Identifieur interne : 000514 ( Pmc/Corpus ); précédent : 000513; suivant : 000515IL-27 promotes IL-10 production by effector Th1 CD4+ T cells; a critical mechanism for protection from severe immunopathology during malaria infection1
Auteurs : Ana Paula Freitas Do Rosário ; Tracey Lamb ; Philip Spence ; Robin Stephens ; Agathe Lang ; Axel Roers ; Werner Muller ; Anne O Arra ; Jean LanghorneSource :
- Journal of immunology (Baltimore, Md. : 1950) [ 0022-1767 ] ; 2011.
Abstract
Infection with the malaria parasite,
Url:
DOI: 10.4049/jimmunol.1102755
PubMed: 22205023
PubMed Central: 3272378
Links to Exploration step
PMC:3272378Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">IL-27 promotes IL-10 production by effector Th1 CD4<sup>+</sup>
T cells; a critical mechanism for protection from severe immunopathology during malaria infection<sup><xref ref-type="fn" rid="FN1">1</xref>
</sup>
</title>
<author><name sortKey="Freitas Do Rosario, Ana Paula" sort="Freitas Do Rosario, Ana Paula" uniqKey="Freitas Do Rosario A" first="Ana Paula" last="Freitas Do Rosário">Ana Paula Freitas Do Rosário</name>
<affiliation><nlm:aff id="A1">Divisions of Parasitology, MRC National Institute for Medical Research, London, UK</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Lamb, Tracey" sort="Lamb, Tracey" uniqKey="Lamb T" first="Tracey" last="Lamb">Tracey Lamb</name>
<affiliation><nlm:aff id="A1">Divisions of Parasitology, MRC National Institute for Medical Research, London, UK</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Spence, Philip" sort="Spence, Philip" uniqKey="Spence P" first="Philip" last="Spence">Philip Spence</name>
<affiliation><nlm:aff id="A1">Divisions of Parasitology, MRC National Institute for Medical Research, London, UK</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Stephens, Robin" sort="Stephens, Robin" uniqKey="Stephens R" first="Robin" last="Stephens">Robin Stephens</name>
<affiliation><nlm:aff id="A1">Divisions of Parasitology, MRC National Institute for Medical Research, London, UK</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Lang, Agathe" sort="Lang, Agathe" uniqKey="Lang A" first="Agathe" last="Lang">Agathe Lang</name>
<affiliation><nlm:aff id="A1">Divisions of Parasitology, MRC National Institute for Medical Research, London, UK</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Roers, Axel" sort="Roers, Axel" uniqKey="Roers A" first="Axel" last="Roers">Axel Roers</name>
<affiliation><nlm:aff id="A3">Medical Faculty Carl Gustav Carus, University of Technology Dresden, Dresden, Germany</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Muller, Werner" sort="Muller, Werner" uniqKey="Muller W" first="Werner" last="Muller">Werner Muller</name>
<affiliation><nlm:aff id="A4">Faculty of Life Sciences, University of Manchester, Manchester, UK.</nlm:aff>
</affiliation>
</author>
<author><name sortKey="O Arra, Anne" sort="O Arra, Anne" uniqKey="O Arra A" first="Anne" last="O Arra">Anne O Arra</name>
<affiliation><nlm:aff id="A2">Immunoregulation, MRC National Institute for Medical Research, London, UK</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Langhorne, Jean" sort="Langhorne, Jean" uniqKey="Langhorne J" first="Jean" last="Langhorne">Jean Langhorne</name>
<affiliation><nlm:aff id="A1">Divisions of Parasitology, MRC National Institute for Medical Research, London, UK</nlm:aff>
</affiliation>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">PMC</idno>
<idno type="pmid">22205023</idno>
<idno type="pmc">3272378</idno>
<idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3272378</idno>
<idno type="RBID">PMC:3272378</idno>
<idno type="doi">10.4049/jimmunol.1102755</idno>
<date when="2011">2011</date>
<idno type="wicri:Area/Pmc/Corpus">000514</idno>
<idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000514</idno>
</publicationStmt>
<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">IL-27 promotes IL-10 production by effector Th1 CD4<sup>+</sup>
T cells; a critical mechanism for protection from severe immunopathology during malaria infection<sup><xref ref-type="fn" rid="FN1">1</xref>
</sup>
</title>
<author><name sortKey="Freitas Do Rosario, Ana Paula" sort="Freitas Do Rosario, Ana Paula" uniqKey="Freitas Do Rosario A" first="Ana Paula" last="Freitas Do Rosário">Ana Paula Freitas Do Rosário</name>
<affiliation><nlm:aff id="A1">Divisions of Parasitology, MRC National Institute for Medical Research, London, UK</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Lamb, Tracey" sort="Lamb, Tracey" uniqKey="Lamb T" first="Tracey" last="Lamb">Tracey Lamb</name>
<affiliation><nlm:aff id="A1">Divisions of Parasitology, MRC National Institute for Medical Research, London, UK</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Spence, Philip" sort="Spence, Philip" uniqKey="Spence P" first="Philip" last="Spence">Philip Spence</name>
<affiliation><nlm:aff id="A1">Divisions of Parasitology, MRC National Institute for Medical Research, London, UK</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Stephens, Robin" sort="Stephens, Robin" uniqKey="Stephens R" first="Robin" last="Stephens">Robin Stephens</name>
<affiliation><nlm:aff id="A1">Divisions of Parasitology, MRC National Institute for Medical Research, London, UK</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Lang, Agathe" sort="Lang, Agathe" uniqKey="Lang A" first="Agathe" last="Lang">Agathe Lang</name>
<affiliation><nlm:aff id="A1">Divisions of Parasitology, MRC National Institute for Medical Research, London, UK</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Roers, Axel" sort="Roers, Axel" uniqKey="Roers A" first="Axel" last="Roers">Axel Roers</name>
<affiliation><nlm:aff id="A3">Medical Faculty Carl Gustav Carus, University of Technology Dresden, Dresden, Germany</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Muller, Werner" sort="Muller, Werner" uniqKey="Muller W" first="Werner" last="Muller">Werner Muller</name>
<affiliation><nlm:aff id="A4">Faculty of Life Sciences, University of Manchester, Manchester, UK.</nlm:aff>
</affiliation>
</author>
<author><name sortKey="O Arra, Anne" sort="O Arra, Anne" uniqKey="O Arra A" first="Anne" last="O Arra">Anne O Arra</name>
<affiliation><nlm:aff id="A2">Immunoregulation, MRC National Institute for Medical Research, London, UK</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Langhorne, Jean" sort="Langhorne, Jean" uniqKey="Langhorne J" first="Jean" last="Langhorne">Jean Langhorne</name>
<affiliation><nlm:aff id="A1">Divisions of Parasitology, MRC National Institute for Medical Research, London, UK</nlm:aff>
</affiliation>
</author>
</analytic>
<series><title level="j">Journal of immunology (Baltimore, Md. : 1950)</title>
<idno type="ISSN">0022-1767</idno>
<idno type="eISSN">1550-6606</idno>
<imprint><date when="2011">2011</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc><textClass></textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en"><p id="P3">Infection with the malaria parasite, <italic>Plasmodium</italic>
, is characterized by excessive inflammation. The establishment of a precise balance between the pro- and anti-inflammatory responses is critical to guarantee control of the parasite and survival of the host. Interleukin (IL)-10, a key regulatory cytokine produced by many cells of the immune system, has been shown to protect mice against pathology during acute <italic>Plasmodium chabaudi chabaudi</italic>
AS model of malaria. However, the critical cellular source of IL-10 is still unknown. Here, we demonstrate that T cell-derived IL-10 is necessary for the control of pathology during acute malaria, as mice bearing specific deletion of <italic>Il10</italic>
in T cells fully reproduce the phenotype observed in <italic>Il10</italic>
<sup>−/−</sup>
mice, with significant weight loss, drop in temperature and increased mortality. Furthermore, we show that IFN-γ<sup>+</sup>
Th1 cells are the main producers of IL-10 throughout acute infection, expressing high levels of CD44 and ICOS and low levels of CD127. Although Foxp3<sup>+</sup>
regulatory CD4<sup>+</sup>
T cells produce IL-10 during infection, highly activated IFN-γ<sup>+</sup>
Th1 cells were shown to be the essential and sufficient source of IL-10 to guarantee protection against severe immune-mediated pathology. Finally, in this model of malaria we demonstrate that the generation of protective IL10<sup>+</sup>
IFN-γ<sup>+</sup>
Th1 cells is dependent on IL-27 signaling, and independent of IL-21.</p>
</div>
</front>
</TEI>
<pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<pmc-dir>properties manuscript</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-journal-id">2985117R</journal-id>
<journal-id journal-id-type="pubmed-jr-id">4816</journal-id>
<journal-id journal-id-type="nlm-ta">J Immunol</journal-id>
<journal-id journal-id-type="iso-abbrev">J. Immunol.</journal-id>
<journal-title-group><journal-title>Journal of immunology (Baltimore, Md. : 1950)</journal-title>
</journal-title-group>
<issn pub-type="ppub">0022-1767</issn>
<issn pub-type="epub">1550-6606</issn>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">22205023</article-id>
<article-id pub-id-type="pmc">3272378</article-id>
<article-id pub-id-type="doi">10.4049/jimmunol.1102755</article-id>
<article-id pub-id-type="manuscript">UKMS40427</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Article</subject>
</subj-group>
</article-categories>
<title-group><article-title>IL-27 promotes IL-10 production by effector Th1 CD4<sup>+</sup>
T cells; a critical mechanism for protection from severe immunopathology during malaria infection<sup><xref ref-type="fn" rid="FN1">1</xref>
</sup>
</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Freitas do Rosário</surname>
<given-names>Ana Paula</given-names>
</name>
<xref ref-type="aff" rid="A1">*</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Lamb</surname>
<given-names>Tracey</given-names>
</name>
<xref ref-type="aff" rid="A1">*</xref>
<xref ref-type="author-notes" rid="FN2">†</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Spence</surname>
<given-names>Philip</given-names>
</name>
<xref ref-type="aff" rid="A1">*</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Stephens</surname>
<given-names>Robin</given-names>
</name>
<xref ref-type="aff" rid="A1">*</xref>
<xref ref-type="author-notes" rid="FN3">‡</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Lang</surname>
<given-names>Agathe</given-names>
</name>
<xref ref-type="aff" rid="A1">*</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Roers</surname>
<given-names>Axel</given-names>
</name>
<xref ref-type="aff" rid="A3">§</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Muller</surname>
<given-names>Werner</given-names>
</name>
<xref ref-type="aff" rid="A4">¶</xref>
</contrib>
<contrib contrib-type="author"><name><surname>O’Garra</surname>
<given-names>Anne</given-names>
</name>
<xref ref-type="aff" rid="A2">||</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Langhorne</surname>
<given-names>Jean</given-names>
</name>
<xref ref-type="aff" rid="A1">*</xref>
</contrib>
</contrib-group>
<aff id="A1"><label>*</label>
Divisions of Parasitology, MRC National Institute for Medical Research, London, UK</aff>
<aff id="A2"><label>||</label>
Immunoregulation, MRC National Institute for Medical Research, London, UK</aff>
<aff id="A3"><label>§</label>
Medical Faculty Carl Gustav Carus, University of Technology Dresden, Dresden, Germany</aff>
<aff id="A4"><label>¶</label>
Faculty of Life Sciences, University of Manchester, Manchester, UK.</aff>
<author-notes><corresp id="CR1">Corresponding author: Jean Langhorne, Division of Parasitology, National Institute for Medical Research, The Ridgeway, London NW7 1AA. <email>jlangho@nimr.mrc.ac.uk</email>
, tel: +44 208 816 2558.</corresp>
<fn fn-type="present-address" id="FN2"><label>†</label>
<p id="P1">Current address: Division of Pediatric infectious Diseases, Emory University School of Medicine, Georgia, USA.</p>
</fn>
<fn fn-type="present-address" id="FN3"><label>‡</label>
<p id="P2">Current address: Department of Internal Medicine, Division of Infectious Diseases, University of Texas Medical Branch, Texas, USA.</p>
</fn>
</author-notes>
<pub-date pub-type="nihms-submitted"><day>12</day>
<month>1</month>
<year>2012</year>
</pub-date>
<pub-date pub-type="epub"><day>28</day>
<month>12</month>
<year>2011</year>
</pub-date>
<pub-date pub-type="ppub"><day>1</day>
<month>2</month>
<year>2012</year>
</pub-date>
<pub-date pub-type="pmc-release"><day>01</day>
<month>8</month>
<year>2012</year>
</pub-date>
<volume>188</volume>
<issue>3</issue>
<fpage>1178</fpage>
<lpage>1190</lpage>
<abstract><p id="P3">Infection with the malaria parasite, <italic>Plasmodium</italic>
, is characterized by excessive inflammation. The establishment of a precise balance between the pro- and anti-inflammatory responses is critical to guarantee control of the parasite and survival of the host. Interleukin (IL)-10, a key regulatory cytokine produced by many cells of the immune system, has been shown to protect mice against pathology during acute <italic>Plasmodium chabaudi chabaudi</italic>
AS model of malaria. However, the critical cellular source of IL-10 is still unknown. Here, we demonstrate that T cell-derived IL-10 is necessary for the control of pathology during acute malaria, as mice bearing specific deletion of <italic>Il10</italic>
in T cells fully reproduce the phenotype observed in <italic>Il10</italic>
<sup>−/−</sup>
mice, with significant weight loss, drop in temperature and increased mortality. Furthermore, we show that IFN-γ<sup>+</sup>
Th1 cells are the main producers of IL-10 throughout acute infection, expressing high levels of CD44 and ICOS and low levels of CD127. Although Foxp3<sup>+</sup>
regulatory CD4<sup>+</sup>
T cells produce IL-10 during infection, highly activated IFN-γ<sup>+</sup>
Th1 cells were shown to be the essential and sufficient source of IL-10 to guarantee protection against severe immune-mediated pathology. Finally, in this model of malaria we demonstrate that the generation of protective IL10<sup>+</sup>
IFN-γ<sup>+</sup>
Th1 cells is dependent on IL-27 signaling, and independent of IL-21.</p>
</abstract>
<funding-group><award-group><funding-source country="United Kingdom">Wellcome Trust : </funding-source>
<award-id>089553 || WT</award-id>
</award-group>
<award-group><funding-source country="United Kingdom">Medical Research Council : </funding-source>
<award-id>U.1175.02.004.00004(60507) || MRC_</award-id>
</award-group>
</funding-group>
</article-meta>
</front>
</pmc>
</record>
Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Sante/explor/CovidV1/Data/Pmc/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000514 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Pmc/Corpus/biblio.hfd -nk 000514 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien |wiki= Wicri/Sante |area= CovidV1 |flux= Pmc |étape= Corpus |type= RBID |clé= PMC:3272378 |texte= IL-27 promotes IL-10 production by effector Th1 CD4+ T cells; a critical mechanism for protection from severe immunopathology during malaria infection1 }}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/Pmc/Corpus/RBID.i -Sk "pubmed:22205023" \ | HfdSelect -Kh $EXPLOR_AREA/Data/Pmc/Corpus/biblio.hfd \ | NlmPubMed2Wicri -a CovidV1
This area was generated with Dilib version V0.6.33. |