ESAT-6–dependent cytosolic pattern recognition drives noncognate tuberculosis control in vivo
Identifieur interne : 000448 ( Pmc/Corpus ); précédent : 000447; suivant : 000449ESAT-6–dependent cytosolic pattern recognition drives noncognate tuberculosis control in vivo
Auteurs : Andreas Kupz ; Ulrike Zedler ; Manuela St Ber ; Carolina Perdomo ; Anca Dorhoi ; Roland Brosch ; Stefan H. E. KaufmannSource :
- The Journal of Clinical Investigation [ 0021-9738 ] ; ????.
Abstract
IFN-γ is a critical mediator of host defense against
Url:
DOI: 10.1172/JCI84978
PubMed: 27111234
PubMed Central: 4887189
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PMC:4887189Le document en format XML
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<author><name sortKey="Kupz, Andreas" sort="Kupz, Andreas" uniqKey="Kupz A" first="Andreas" last="Kupz">Andreas Kupz</name>
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<author><name sortKey="Zedler, Ulrike" sort="Zedler, Ulrike" uniqKey="Zedler U" first="Ulrike" last="Zedler">Ulrike Zedler</name>
<affiliation><nlm:aff id="A1">Max Planck Institute for Infection Biology, Berlin, Germany.</nlm:aff>
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<author><name sortKey="St Ber, Manuela" sort="St Ber, Manuela" uniqKey="St Ber M" first="Manuela" last="St Ber">Manuela St Ber</name>
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<author><name sortKey="Perdomo, Carolina" sort="Perdomo, Carolina" uniqKey="Perdomo C" first="Carolina" last="Perdomo">Carolina Perdomo</name>
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<author><name sortKey="Dorhoi, Anca" sort="Dorhoi, Anca" uniqKey="Dorhoi A" first="Anca" last="Dorhoi">Anca Dorhoi</name>
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<author><name sortKey="Brosch, Roland" sort="Brosch, Roland" uniqKey="Brosch R" first="Roland" last="Brosch">Roland Brosch</name>
<affiliation><nlm:aff id="A3">Institut Pasteur, Unit for Integrated Mycobacterial Pathogenomics, Paris, France.</nlm:aff>
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<author><name sortKey="Kaufmann, Stefan H E" sort="Kaufmann, Stefan H E" uniqKey="Kaufmann S" first="Stefan H. E." last="Kaufmann">Stefan H. E. Kaufmann</name>
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">ESAT-6–dependent cytosolic pattern recognition drives noncognate tuberculosis control in vivo</title>
<author><name sortKey="Kupz, Andreas" sort="Kupz, Andreas" uniqKey="Kupz A" first="Andreas" last="Kupz">Andreas Kupz</name>
<affiliation><nlm:aff id="A1">Max Planck Institute for Infection Biology, Berlin, Germany.</nlm:aff>
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<author><name sortKey="Zedler, Ulrike" sort="Zedler, Ulrike" uniqKey="Zedler U" first="Ulrike" last="Zedler">Ulrike Zedler</name>
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<author><name sortKey="St Ber, Manuela" sort="St Ber, Manuela" uniqKey="St Ber M" first="Manuela" last="St Ber">Manuela St Ber</name>
<affiliation><nlm:aff id="A1">Max Planck Institute for Infection Biology, Berlin, Germany.</nlm:aff>
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<author><name sortKey="Perdomo, Carolina" sort="Perdomo, Carolina" uniqKey="Perdomo C" first="Carolina" last="Perdomo">Carolina Perdomo</name>
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<author><name sortKey="Dorhoi, Anca" sort="Dorhoi, Anca" uniqKey="Dorhoi A" first="Anca" last="Dorhoi">Anca Dorhoi</name>
<affiliation><nlm:aff id="A1">Max Planck Institute for Infection Biology, Berlin, Germany.</nlm:aff>
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<author><name sortKey="Brosch, Roland" sort="Brosch, Roland" uniqKey="Brosch R" first="Roland" last="Brosch">Roland Brosch</name>
<affiliation><nlm:aff id="A3">Institut Pasteur, Unit for Integrated Mycobacterial Pathogenomics, Paris, France.</nlm:aff>
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<series><title level="j">The Journal of Clinical Investigation</title>
<idno type="ISSN">0021-9738</idno>
<idno type="eISSN">1558-8238</idno>
<imprint><date when="????">????</date>
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<front><div type="abstract" xml:lang="en"><p>IFN-γ is a critical mediator of host defense against <italic>Mycobacterium tuberculosis</italic>
(<italic>Mtb</italic>
) infection. Antigen-specific CD4<sup>+</sup>
T cells have long been regarded as the main producer of IFN-γ in tuberculosis (TB), and CD4<sup>+</sup>
T cell immunity is the main target of current TB vaccine candidates. However, given the recent failures of such a TB vaccine candidate in clinical trials, strategies to harness CD4-independent mechanisms of protection should be included in future vaccine design. Here, we have reported that noncognate IFN-γ production by <italic>Mtb</italic>
antigen–independent memory CD8<sup>+</sup>
T cells and NK cells is protective during <italic>Mtb</italic>
infection and evaluated the mechanistic regulation of IFN-γ production by these cells in vivo. Transfer of arenavirus- or protein-specific CD8<sup>+</sup>
T cells or NK cells reduced the mortality and morbidity rates of mice highly susceptible to TB in an IFN-γ–dependent manner. Secretion of IFN-γ by these cell populations required IL-18, sensing of mycobacterial viability, <italic>Mtb</italic>
protein 6-kDa early secretory antigenic target–mediated (ESAT-6–mediated) cytosolic contact, and activation of NLR family pyrin domain–containing protein 3 (NLRP3) inflammasomes in CD11c<sup>+</sup>
cell subsets. Neutralization of IL-18 abrogated protection in susceptible recipient mice that had received noncognate cells. Moreover, improved <italic>Mycobacterium</italic>
<italic>bovis</italic>
bacillus Calmette-Guérin (BCG) vaccine–induced protection was lost in the absence of ESAT-6–dependent cytosolic contact. Our findings provide a comprehensive mechanistic framework for antigen-independent IFN-γ secretion in response to <italic>Mt</italic>
b with critical implications for future intervention strategies against TB.</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>
<front><journal-meta><journal-id journal-id-type="nlm-ta">J Clin Invest</journal-id>
<journal-id journal-id-type="iso-abbrev">J. Clin. Invest</journal-id>
<journal-id journal-id-type="publisher-id">J Clin Invest</journal-id>
<journal-title-group><journal-title>The Journal of Clinical Investigation</journal-title>
</journal-title-group>
<issn pub-type="ppub">0021-9738</issn>
<issn pub-type="epub">1558-8238</issn>
<publisher><publisher-name>American Society for Clinical Investigation</publisher-name>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">27111234</article-id>
<article-id pub-id-type="pmc">4887189</article-id>
<article-id pub-id-type="publisher-id">84978</article-id>
<article-id pub-id-type="doi">10.1172/JCI84978</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Research Article</subject>
</subj-group>
</article-categories>
<title-group><article-title>ESAT-6–dependent cytosolic pattern recognition drives noncognate tuberculosis control in vivo</article-title>
</title-group>
<contrib-group><contrib contrib-type="author" corresp="yes"><name><surname>Kupz</surname>
<given-names>Andreas</given-names>
</name>
<email>kupz@mpiib-berlin.mpg.de</email>
<xref ref-type="aff" rid="A1">1</xref>
<xref ref-type="aff" rid="A2">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Zedler</surname>
<given-names>Ulrike</given-names>
</name>
<email>zedler@mpiib-berlin.mpg.de</email>
<xref ref-type="aff" rid="A1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Stäber</surname>
<given-names>Manuela</given-names>
</name>
<email>staeber@mpiib-berlin.mpg.de</email>
<xref ref-type="aff" rid="A1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Perdomo</surname>
<given-names>Carolina</given-names>
</name>
<email>perdomo@mpiib-berlin.mpg.de</email>
<xref ref-type="aff" rid="A1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Dorhoi</surname>
<given-names>Anca</given-names>
</name>
<email>dorhoi@mpiib-berlin.mpg.de</email>
<xref ref-type="aff" rid="A1">1</xref>
</contrib>
<contrib contrib-type="author"><contrib-id contrib-id-type="orcid" authenticated="true">http://orcid.org/0000-0003-2587-3863</contrib-id>
<name><surname>Brosch</surname>
<given-names>Roland</given-names>
</name>
<email>rbrosch@pasteur.fr</email>
<xref ref-type="aff" rid="A3">3</xref>
</contrib>
<contrib contrib-type="author"><contrib-id contrib-id-type="orcid" authenticated="true">http://orcid.org/0000-0001-9866-8268</contrib-id>
<name><surname>Kaufmann</surname>
<given-names>Stefan H.E.</given-names>
</name>
<email>kaufmann@mpiib-berlin.mpg.de</email>
<xref ref-type="aff" rid="A1">1</xref>
</contrib>
</contrib-group>
<aff id="A1"><label>1</label>
Max Planck Institute for Infection Biology, Berlin, Germany.</aff>
<aff id="A2"><label>2</label>
Centre for Biosecurity and Tropical Infectious Diseases, Australian Institute of Tropical Health and Medicine, James Cook University, Cairns, Queensland, Australia.</aff>
<aff id="A3"><label>3</label>
Institut Pasteur, Unit for Integrated Mycobacterial Pathogenomics, Paris, France.</aff>
<author-notes><corresp>Address correspondence to: Stefan H.E. Kaufmann or Andreas Kupz, Max Plank Institute for Infection Biology, Charitéplatz 1, 10117, Berlin, Germany. Phone: 49.30.28460.500; E-mail: <email>kaufmann@mpiib-berlin.mpg.de</email>
. Phone: 49.30.28460.520; E-mail: <email>kupz@mpiib-berlin.mpg.de</email>
or <email>andreas.kupz@jcu.edu.au</email>
.</corresp>
</author-notes>
<pub-date date-type="pub" publication-format="electronic" iso-8601-date="2016-04-25"><day>25</day>
<month>4</month>
<year>2016</year>
</pub-date>
<pub-date date-type="pub" publication-format="print" iso-8601-date="2016-06-01"><day>1</day>
<month>6</month>
<year>2016</year>
</pub-date>
<pub-date pub-type="pmc-release"><day>1</day>
<month>9</month>
<year>2016</year>
</pub-date>
<pmc-comment> PMC Release delay is 3 months and
0 days and was based on the . </pmc-comment>
<volume>126</volume>
<issue>6</issue>
<fpage>2109</fpage>
<lpage>2122</lpage>
<history><date date-type="received"><day>5</day>
<month>10</month>
<year>2015</year>
</date>
<date date-type="accepted"><day>8</day>
<month>3</month>
<year>2016</year>
</date>
</history>
<permissions><copyright-statement>Copyright © 2016, American Society for Clinical Investigation</copyright-statement>
<copyright-year>2016</copyright-year>
<copyright-holder>American Society for Clinical Investigation</copyright-holder>
</permissions>
<self-uri xlink:href="https://www.jci.org/articles/view/84978">This article is available online at https://www.jci.org/articles/view/84978</self-uri>
<abstract><p>IFN-γ is a critical mediator of host defense against <italic>Mycobacterium tuberculosis</italic>
(<italic>Mtb</italic>
) infection. Antigen-specific CD4<sup>+</sup>
T cells have long been regarded as the main producer of IFN-γ in tuberculosis (TB), and CD4<sup>+</sup>
T cell immunity is the main target of current TB vaccine candidates. However, given the recent failures of such a TB vaccine candidate in clinical trials, strategies to harness CD4-independent mechanisms of protection should be included in future vaccine design. Here, we have reported that noncognate IFN-γ production by <italic>Mtb</italic>
antigen–independent memory CD8<sup>+</sup>
T cells and NK cells is protective during <italic>Mtb</italic>
infection and evaluated the mechanistic regulation of IFN-γ production by these cells in vivo. Transfer of arenavirus- or protein-specific CD8<sup>+</sup>
T cells or NK cells reduced the mortality and morbidity rates of mice highly susceptible to TB in an IFN-γ–dependent manner. Secretion of IFN-γ by these cell populations required IL-18, sensing of mycobacterial viability, <italic>Mtb</italic>
protein 6-kDa early secretory antigenic target–mediated (ESAT-6–mediated) cytosolic contact, and activation of NLR family pyrin domain–containing protein 3 (NLRP3) inflammasomes in CD11c<sup>+</sup>
cell subsets. Neutralization of IL-18 abrogated protection in susceptible recipient mice that had received noncognate cells. Moreover, improved <italic>Mycobacterium</italic>
<italic>bovis</italic>
bacillus Calmette-Guérin (BCG) vaccine–induced protection was lost in the absence of ESAT-6–dependent cytosolic contact. Our findings provide a comprehensive mechanistic framework for antigen-independent IFN-γ secretion in response to <italic>Mt</italic>
b with critical implications for future intervention strategies against TB.</p>
</abstract>
</article-meta>
</front>
</pmc>
</record>
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