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rdf:type |
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lifeskim:mentions |
umls-concept:C0004368,
umls-concept:C0962189,
umls-concept:C0962190,
umls-concept:C1149199,
umls-concept:C1149231,
umls-concept:C1334107,
umls-concept:C1367171,
umls-concept:C1416406,
umls-concept:C1423038,
umls-concept:C1515655,
umls-concept:C1527148,
umls-concept:C1611645,
umls-concept:C1831593,
umls-concept:C2936411
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pubmed:issue |
7
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pubmed:dateCreated |
2008-7-1
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pubmed:abstractText |
Th17 cells have been recognized as the central effectors in organ-related autoimmune diseases. IL-6 is a key factor that reciprocally regulates Th17 and Foxp3(+) Treg differentiation by inhibition of TGF-beta induced Foxp3 and induction of RORgammat, a Th17 lineage-specific transcription factor. Recently IL-21 has been suggested to induce RORgammat and Th17 development in the absence of IL-6. However, the relevance of IL-21 for Th17-dependent inflammatory responses in vivo remains unclear. In this study, we demonstrate that differentiation of IL-17-producing CD4 T cells, their recruitment to inflamed organs, and the development of autoimmune disease was not affected in il21R(-/-) and il21(-/-) mice in models of myelin oligodendrocyte glycoprotein-induced autoimmune encephalitis and autoimmune myocarditis. IL-6 induced Th17 differentiation independent of and much more potently than IL-21 in vitro. These data suggest that IL-6 is sufficient to drive Th17 development and associated autoimmunity in vivo in the absence of IL-21 or IL-21R.
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pubmed:commentsCorrections |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-17,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-6,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukins,
http://linkedlifedata.com/resource/pubmed/chemical/Nuclear Receptor Subfamily 1...,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin-21,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Retinoic Acid,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Thyroid Hormone,
http://linkedlifedata.com/resource/pubmed/chemical/Rorc protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Transforming Growth Factor beta,
http://linkedlifedata.com/resource/pubmed/chemical/interleukin-21
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
0014-2980
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
38
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1833-8
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:18546146-Animals,
pubmed-meshheading:18546146-Autoimmune Diseases,
pubmed-meshheading:18546146-Autoimmunity,
pubmed-meshheading:18546146-Disease Models, Animal,
pubmed-meshheading:18546146-Encephalomyelitis, Autoimmune, Experimental,
pubmed-meshheading:18546146-Interleukin-17,
pubmed-meshheading:18546146-Interleukin-6,
pubmed-meshheading:18546146-Interleukins,
pubmed-meshheading:18546146-Mice,
pubmed-meshheading:18546146-Mice, Inbred BALB C,
pubmed-meshheading:18546146-Mice, Inbred C57BL,
pubmed-meshheading:18546146-Mice, Knockout,
pubmed-meshheading:18546146-Myocarditis,
pubmed-meshheading:18546146-Nervous System Autoimmune Disease, Experimental,
pubmed-meshheading:18546146-Nuclear Receptor Subfamily 1, Group F, Member 3,
pubmed-meshheading:18546146-Receptors, Interleukin-21,
pubmed-meshheading:18546146-Receptors, Retinoic Acid,
pubmed-meshheading:18546146-Receptors, Thyroid Hormone,
pubmed-meshheading:18546146-T-Lymphocytes, Helper-Inducer,
pubmed-meshheading:18546146-T-Lymphocytes, Regulatory,
pubmed-meshheading:18546146-Transforming Growth Factor beta
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pubmed:year |
2008
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pubmed:articleTitle |
IL-21 and IL-21R are not required for development of Th17 cells and autoimmunity in vivo.
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pubmed:affiliation |
Institute of Integrative Biology, Molecular Biomedicine, ETH Zürich, Zürich, Switzerland.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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