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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">T-bet<sup>+</sup> Treg Cells Undergo Abortive Th1 Cell Differentiation due to Impaired Expression of IL-12 Receptor β2</title><author><name sortKey="Koch, Meghan A" sort="Koch, Meghan A" uniqKey="Koch M" first="Meghan A." last="Koch">Meghan A. Koch</name><affiliation><nlm:aff id="A1">Benaroya Research Institute, Seattle, WA, 98101, USA</nlm:aff></affiliation><affiliation><nlm:aff id="A2">Department of Immunology, University of Washington School of Medicine, Seattle Washington, 98195, USA</nlm:aff></affiliation></author><author><name sortKey="Thomas, Kerri N" sort="Thomas, Kerri N" uniqKey="Thomas K" first="Kerri N." last="Thomas">Kerri N. Thomas</name><affiliation><nlm:aff id="A1">Benaroya Research Institute, Seattle, WA, 98101, USA</nlm:aff></affiliation></author><author><name sortKey="Perdue, Nikole R" sort="Perdue, Nikole R" uniqKey="Perdue N" first="Nikole R." last="Perdue">Nikole R. Perdue</name><affiliation><nlm:aff id="A1">Benaroya Research Institute, Seattle, WA, 98101, USA</nlm:aff></affiliation></author><author><name sortKey="Smigiel, Kate S" sort="Smigiel, Kate S" uniqKey="Smigiel K" first="Kate S." last="Smigiel">Kate S. Smigiel</name><affiliation><nlm:aff id="A1">Benaroya Research Institute, Seattle, WA, 98101, USA</nlm:aff></affiliation><affiliation><nlm:aff id="A2">Department of Immunology, University of Washington School of Medicine, Seattle Washington, 98195, USA</nlm:aff></affiliation></author><author><name sortKey="Srivastava, Shivani" sort="Srivastava, Shivani" uniqKey="Srivastava S" first="Shivani" last="Srivastava">Shivani Srivastava</name><affiliation><nlm:aff id="A1">Benaroya Research Institute, Seattle, WA, 98101, USA</nlm:aff></affiliation><affiliation><nlm:aff id="A2">Department of Immunology, University of Washington School of Medicine, Seattle Washington, 98195, USA</nlm:aff></affiliation></author><author><name sortKey="Campbell, Daniel J" sort="Campbell, Daniel J" uniqKey="Campbell D" first="Daniel J." last="Campbell">Daniel J. Campbell</name><affiliation><nlm:aff id="A1">Benaroya Research Institute, Seattle, WA, 98101, USA</nlm:aff></affiliation><affiliation><nlm:aff id="A2">Department of Immunology, University of Washington School of Medicine, Seattle Washington, 98195, USA</nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">22960221</idno><idno type="pmc">3501343</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3501343</idno><idno type="RBID">PMC:3501343</idno><idno type="doi">10.1016/j.immuni.2012.05.031</idno><date when="2012">2012</date><idno type="wicri:Area/Pmc/Corpus">000790</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000790</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">T-bet<sup>+</sup> Treg Cells Undergo Abortive Th1 Cell Differentiation due to Impaired Expression of IL-12 Receptor β2</title><author><name sortKey="Koch, Meghan A" sort="Koch, Meghan A" uniqKey="Koch M" first="Meghan A." last="Koch">Meghan A. Koch</name><affiliation><nlm:aff id="A1">Benaroya Research Institute, Seattle, WA, 98101, USA</nlm:aff></affiliation><affiliation><nlm:aff id="A2">Department of Immunology, University of Washington School of Medicine, Seattle Washington, 98195, USA</nlm:aff></affiliation></author><author><name sortKey="Thomas, Kerri N" sort="Thomas, Kerri N" uniqKey="Thomas K" first="Kerri N." last="Thomas">Kerri N. Thomas</name><affiliation><nlm:aff id="A1">Benaroya Research Institute, Seattle, WA, 98101, USA</nlm:aff></affiliation></author><author><name sortKey="Perdue, Nikole R" sort="Perdue, Nikole R" uniqKey="Perdue N" first="Nikole R." last="Perdue">Nikole R. Perdue</name><affiliation><nlm:aff id="A1">Benaroya Research Institute, Seattle, WA, 98101, USA</nlm:aff></affiliation></author><author><name sortKey="Smigiel, Kate S" sort="Smigiel, Kate S" uniqKey="Smigiel K" first="Kate S." last="Smigiel">Kate S. Smigiel</name><affiliation><nlm:aff id="A1">Benaroya Research Institute, Seattle, WA, 98101, USA</nlm:aff></affiliation><affiliation><nlm:aff id="A2">Department of Immunology, University of Washington School of Medicine, Seattle Washington, 98195, USA</nlm:aff></affiliation></author><author><name sortKey="Srivastava, Shivani" sort="Srivastava, Shivani" uniqKey="Srivastava S" first="Shivani" last="Srivastava">Shivani Srivastava</name><affiliation><nlm:aff id="A1">Benaroya Research Institute, Seattle, WA, 98101, USA</nlm:aff></affiliation><affiliation><nlm:aff id="A2">Department of Immunology, University of Washington School of Medicine, Seattle Washington, 98195, USA</nlm:aff></affiliation></author><author><name sortKey="Campbell, Daniel J" sort="Campbell, Daniel J" uniqKey="Campbell D" first="Daniel J." last="Campbell">Daniel J. Campbell</name><affiliation><nlm:aff id="A1">Benaroya Research Institute, Seattle, WA, 98101, USA</nlm:aff></affiliation><affiliation><nlm:aff id="A2">Department of Immunology, University of Washington School of Medicine, Seattle Washington, 98195, USA</nlm:aff></affiliation></author></analytic><series><title level="j">Immunity</title><idno type="ISSN">1074-7613</idno><idno type="eISSN">1097-4180</idno><imprint><date when="2012">2012</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><title>SUMMARY</title><p id="P3">Foxp3<sup>+</sup> regulatory T (Treg) cells limit inflammatory responses and maintain immune homeostasis. Although comprised of several phenotypically and functionally distinct subsets, the differentiation of specialized Treg cell populations within the periphery is poorly characterized. We demonstrate that the development of T-bet<sup>+</sup> Treg cells that potently inhibit T helper (Th)1 cell responses was dependent on the transcription factor STAT1, and occurred directly in response to interferon-γ produced by effector T cells. Additionally, delayed induction of the IL-12Rβ2 receptor component following STAT1 activation helped ensure that Treg cells do not readily complete STAT4-dependent Th1 cell development and lose their ability to suppress effector T cell proliferation. Thus, we define a pathway of abortive Th1 cell development that results in the specialization of peripheral Treg cells, and demonstrate that impaired expression of a single cytokine receptor helps maintain Treg cell suppressive function in the context of inflammatory Th1 cell responses.</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">9432918</journal-id><journal-id journal-id-type="pubmed-jr-id">8591</journal-id><journal-id journal-id-type="nlm-ta">Immunity</journal-id><journal-id journal-id-type="iso-abbrev">Immunity</journal-id><journal-title-group><journal-title>Immunity</journal-title></journal-title-group><issn pub-type="ppub">1074-7613</issn><issn pub-type="epub">1097-4180</issn></journal-meta><article-meta><article-id pub-id-type="pmid">22960221</article-id><article-id pub-id-type="pmc">3501343</article-id><article-id pub-id-type="doi">10.1016/j.immuni.2012.05.031</article-id><article-id pub-id-type="manuscript">NIHMS405612</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>T-bet<sup>+</sup> Treg Cells Undergo Abortive Th1 Cell Differentiation due to Impaired Expression of IL-12 Receptor β2</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Koch</surname><given-names>Meghan A.</given-names></name><xref ref-type="aff" rid="A1">1</xref><xref ref-type="aff" rid="A2">2</xref></contrib><contrib contrib-type="author"><name><surname>Thomas</surname><given-names>Kerri N.</given-names></name><xref ref-type="aff" rid="A1">1</xref></contrib><contrib contrib-type="author"><name><surname>Perdue</surname><given-names>Nikole R.</given-names></name><xref ref-type="aff" rid="A1">1</xref></contrib><contrib contrib-type="author"><name><surname>Smigiel</surname><given-names>Kate S.</given-names></name><xref ref-type="aff" rid="A1">1</xref><xref ref-type="aff" rid="A2">2</xref></contrib><contrib contrib-type="author"><name><surname>Srivastava</surname><given-names>Shivani</given-names></name><xref ref-type="aff" rid="A1">1</xref><xref ref-type="aff" rid="A2">2</xref></contrib><contrib contrib-type="author"><name><surname>Campbell</surname><given-names>Daniel J.</given-names></name><xref ref-type="aff" rid="A1">1</xref><xref ref-type="aff" rid="A2">2</xref></contrib></contrib-group><aff id="A1"><label>1</label>Benaroya Research Institute, Seattle, WA, 98101, USA</aff><aff id="A2"><label>2</label>Department of Immunology, University of Washington School of Medicine, Seattle Washington, 98195, USA</aff><author-notes><corresp id="FN1">Correspondence: <email>campbell@benaroyaresearch.org</email></corresp></author-notes><pub-date pub-type="nihms-submitted"><day>10</day><month>9</month><year>2012</year></pub-date><pub-date pub-type="epub"><day>06</day><month>9</month><year>2012</year></pub-date><pub-date pub-type="ppub"><day>21</day><month>9</month><year>2012</year></pub-date><pub-date pub-type="pmc-release"><day>21</day><month>9</month><year>2013</year></pub-date><volume>37</volume><issue>3</issue><fpage>501</fpage><lpage>510</lpage><permissions><copyright-statement>© 2012 Elsevier Inc. All rights reserved.</copyright-statement><copyright-year>2012</copyright-year></permissions><abstract><title>SUMMARY</title><p id="P3">Foxp3<sup>+</sup> regulatory T (Treg) cells limit inflammatory responses and maintain immune homeostasis. Although comprised of several phenotypically and functionally distinct subsets, the differentiation of specialized Treg cell populations within the periphery is poorly characterized. We demonstrate that the development of T-bet<sup>+</sup> Treg cells that potently inhibit T helper (Th)1 cell responses was dependent on the transcription factor STAT1, and occurred directly in response to interferon-γ produced by effector T cells. Additionally, delayed induction of the IL-12Rβ2 receptor component following STAT1 activation helped ensure that Treg cells do not readily complete STAT4-dependent Th1 cell development and lose their ability to suppress effector T cell proliferation. Thus, we define a pathway of abortive Th1 cell development that results in the specialization of peripheral Treg cells, and demonstrate that impaired expression of a single cytokine receptor helps maintain Treg cell suppressive function in the context of inflammatory Th1 cell responses.</p></abstract><funding-group><award-group><funding-source country="United States">National Institute of Arthritis and Musculoskeletal and Skin Diseases : NIAMS</funding-source><award-id>R01 AR055695 || AR</award-id></award-group><award-group><funding-source country="United States">National Institute of Allergy and Infectious Diseases Extramural Activities : NIAID</funding-source><award-id>R01 AI085130 || AI</award-id></award-group><award-group><funding-source country="United States">National Institute of Allergy and Infectious Diseases Extramural Activities : NIAID</funding-source><award-id>R01 AI067750 || AI</award-id></award-group><award-group><funding-source country="United States">National Heart, Lung, and Blood Institute : NHLBI</funding-source><award-id>P01 HL098067 || HL</award-id></award-group></funding-group></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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