T-bet+ Treg Cells Undergo Abortive Th1 Cell Differentiation due to Impaired Expression of IL-12 Receptor β2
Identifieur interne : 000B52 ( Main/Exploration ); précédent : 000B51; suivant : 000B53T-bet+ Treg Cells Undergo Abortive Th1 Cell Differentiation due to Impaired Expression of IL-12 Receptor β2
Auteurs : Meghan A. Koch [États-Unis] ; Kerri N. Thomas [États-Unis] ; Nikole R. Perdue [États-Unis] ; Kate S. Smigiel [États-Unis] ; Shivani Srivastava [États-Unis] ; Daniel J. Campbell [États-Unis]Source :
- Immunity [ 1074-7613 ] ; 2012.
Abstract
Foxp3+ 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+ 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.
Url:
DOI: 10.1016/j.immuni.2012.05.031
PubMed: 22960221
PubMed Central: 3501343
Affiliations:
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Koch</name><affiliation wicri:level="1"><nlm:aff id="A1">Benaroya Research Institute, Seattle, WA, 98101, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Benaroya Research Institute, Seattle, WA, 98101</wicri:regionArea><wicri:noRegion>98101</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:aff id="A2">Department of Immunology, University of Washington School of Medicine, Seattle Washington, 98195, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Immunology, University of Washington School of Medicine, Seattle Washington, 98195</wicri:regionArea><wicri:noRegion>98195</wicri:noRegion></affiliation></author><author><name sortKey="Thomas, Kerri N" sort="Thomas, Kerri N" uniqKey="Thomas K" first="Kerri N." last="Thomas">Kerri N. 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Campbell</name><affiliation wicri:level="1"><nlm:aff id="A1">Benaroya Research Institute, Seattle, WA, 98101, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Benaroya Research Institute, Seattle, WA, 98101</wicri:regionArea><wicri:noRegion>98101</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:aff id="A2">Department of Immunology, University of Washington School of Medicine, Seattle Washington, 98195, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Immunology, University of Washington School of Medicine, Seattle Washington, 98195</wicri:regionArea><wicri:noRegion>98195</wicri:noRegion></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><affiliations><list><country><li>États-Unis</li></country></list><tree><country name="États-Unis"><noRegion><name sortKey="Koch, Meghan A" sort="Koch, Meghan A" uniqKey="Koch M" first="Meghan A." last="Koch">Meghan A. Koch</name></noRegion><name sortKey="Campbell, Daniel J" sort="Campbell, Daniel J" uniqKey="Campbell D" first="Daniel J." last="Campbell">Daniel J. Campbell</name><name sortKey="Campbell, Daniel J" sort="Campbell, Daniel J" uniqKey="Campbell D" first="Daniel J." last="Campbell">Daniel J. Campbell</name><name sortKey="Koch, Meghan A" sort="Koch, Meghan A" uniqKey="Koch M" first="Meghan A." last="Koch">Meghan A. Koch</name><name sortKey="Perdue, Nikole R" sort="Perdue, Nikole R" uniqKey="Perdue N" first="Nikole R." last="Perdue">Nikole R. Perdue</name><name sortKey="Smigiel, Kate S" sort="Smigiel, Kate S" uniqKey="Smigiel K" first="Kate S." last="Smigiel">Kate S. Smigiel</name><name sortKey="Smigiel, Kate S" sort="Smigiel, Kate S" uniqKey="Smigiel K" first="Kate S." last="Smigiel">Kate S. Smigiel</name><name sortKey="Srivastava, Shivani" sort="Srivastava, Shivani" uniqKey="Srivastava S" first="Shivani" last="Srivastava">Shivani Srivastava</name><name sortKey="Srivastava, Shivani" sort="Srivastava, Shivani" uniqKey="Srivastava S" first="Shivani" last="Srivastava">Shivani Srivastava</name><name sortKey="Thomas, Kerri N" sort="Thomas, Kerri N" uniqKey="Thomas K" first="Kerri N." last="Thomas">Kerri N. Thomas</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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