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Article: Glucocorticoid-induced tumor necrosis factor receptor family-related protein exacerbates collagen-induced arthritis by enhancing the expansion of Th17 cells
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TitleGlucocorticoid-induced tumor necrosis factor receptor family-related protein exacerbates collagen-induced arthritis by enhancing the expansion of Th17 cells
 
AuthorsWang, S1 2
Shi, Y1
Yang, M3
Ma, J1
Tian, J1
Chen, J1
Mao, C1
Jiao, Z1
Ko, KH3
Baidoo, SE1
Xu, H1
Hua, Z2
Lu, L2 3
 
Issue Date2012
 
PublisherElsevier Inc.. The Journal's web site is located at http://ajp.amjpathol.org/
 
CitationThe American Journal of Pathology: cellular and molecular biology of disease, 2012, v. 180 n. 3, p. 1059-1067 [How to Cite?]
DOI: http://dx.doi.org/10.1016/j.ajpath.2011.11.018
 
AbstractRheumatoid arthritis (RA), a chronic autoimmune form of inflammatory joint disease, progressively affects multiple joints with pathological changes in the synovia, cartilage, and bone. Numerous studies have suggested a critical role for glucocorticoid-induced tumor necrosis factor receptor family-related protein (GITR) in the pathogenesis of autoimmune arthritis by modulating both innate and adaptive immune reactions, but the underlying mechanisms by which GITR activation promotes arthritic progression remain largely unclear. In this study, we found that collagen-induced arthritis mice treated with the ligand of GITR (GITRL) displayed an earlier onset of arthritis with a markedly increased severity of arthritic symptoms and joint damage, in which significantly increased Th17 cells in both spleen and draining lymph nodes were observed. Notably, results showed that a marked expansion of Th17 cells with increased RORgammat mRNA expression was induced from naive CD4(+) T cells when cultured with GITRL. Consistently, normal mice that were treated with GITRL were found to display a substantial expansion of splenic Th17 cells. Furthermore, we detected elevated serum levels of GITRL in patients with RA, which were positively correlated with an increase in interleukin-17 production. Taken together, the results from this study have revealed a new function of GITRL in exacerbating autoimmune arthritis via the enhancement of the expansion of Th17 cells.
 
ISSN0002-9440
2013 Impact Factor: 4.602
 
DOIhttp://dx.doi.org/10.1016/j.ajpath.2011.11.018
 
ISI Accession Number IDWOS:000301022200019
 
DC FieldValue
dc.contributor.authorWang, S
 
dc.contributor.authorShi, Y
 
dc.contributor.authorYang, M
 
dc.contributor.authorMa, J
 
dc.contributor.authorTian, J
 
dc.contributor.authorChen, J
 
dc.contributor.authorMao, C
 
dc.contributor.authorJiao, Z
 
dc.contributor.authorKo, KH
 
dc.contributor.authorBaidoo, SE
 
dc.contributor.authorXu, H
 
dc.contributor.authorHua, Z
 
dc.contributor.authorLu, L
 
dc.date.accessioned2012-09-20T08:10:43Z
 
dc.date.available2012-09-20T08:10:43Z
 
dc.date.issued2012
 
dc.description.abstractRheumatoid arthritis (RA), a chronic autoimmune form of inflammatory joint disease, progressively affects multiple joints with pathological changes in the synovia, cartilage, and bone. Numerous studies have suggested a critical role for glucocorticoid-induced tumor necrosis factor receptor family-related protein (GITR) in the pathogenesis of autoimmune arthritis by modulating both innate and adaptive immune reactions, but the underlying mechanisms by which GITR activation promotes arthritic progression remain largely unclear. In this study, we found that collagen-induced arthritis mice treated with the ligand of GITR (GITRL) displayed an earlier onset of arthritis with a markedly increased severity of arthritic symptoms and joint damage, in which significantly increased Th17 cells in both spleen and draining lymph nodes were observed. Notably, results showed that a marked expansion of Th17 cells with increased RORgammat mRNA expression was induced from naive CD4(+) T cells when cultured with GITRL. Consistently, normal mice that were treated with GITRL were found to display a substantial expansion of splenic Th17 cells. Furthermore, we detected elevated serum levels of GITRL in patients with RA, which were positively correlated with an increase in interleukin-17 production. Taken together, the results from this study have revealed a new function of GITRL in exacerbating autoimmune arthritis via the enhancement of the expansion of Th17 cells.
 
dc.identifier.citationThe American Journal of Pathology: cellular and molecular biology of disease, 2012, v. 180 n. 3, p. 1059-1067 [How to Cite?]
DOI: http://dx.doi.org/10.1016/j.ajpath.2011.11.018
 
dc.identifier.citeulike10625413
 
dc.identifier.doihttp://dx.doi.org/10.1016/j.ajpath.2011.11.018
 
dc.identifier.epage1067
 
dc.identifier.hkuros208155
 
dc.identifier.isiWOS:000301022200019
 
dc.identifier.issn0002-9440
2013 Impact Factor: 4.602
 
dc.identifier.issue3
 
dc.identifier.openurl
 
dc.identifier.pmid22214837
 
dc.identifier.scopuseid_2-s2.0-84863171449
 
dc.identifier.spage1059
 
dc.identifier.urihttp://hdl.handle.net/10722/164840
 
dc.identifier.volume180
 
dc.languageeng
 
dc.publisherElsevier Inc.. The Journal's web site is located at http://ajp.amjpathol.org/
 
dc.publisher.placeUnited States
 
dc.relation.ispartofThe American Journal of Pathology: cellular and molecular biology of disease
 
dc.rightsNOTICE: this is the author’s version of a work that was accepted for publication in . Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in PUBLICATION, [VOL#, ISSUE#, (DATE)] DOI#
 
dc.subject.meshArthritis, Experimental - etiology - pathology
 
dc.subject.meshCD4-Positive T-Lymphocytes - metabolism
 
dc.subject.meshCell Differentiation
 
dc.subject.meshGlucocorticoid-Induced TNFR-Related Protein - metabolism - pharmacology - physiology
 
dc.subject.meshTh17 Cells - metabolism - pathology
 
dc.titleGlucocorticoid-induced tumor necrosis factor receptor family-related protein exacerbates collagen-induced arthritis by enhancing the expansion of Th17 cells
 
dc.typeArticle
 
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<contributor.author>Tian, J</contributor.author>
<contributor.author>Chen, J</contributor.author>
<contributor.author>Mao, C</contributor.author>
<contributor.author>Jiao, Z</contributor.author>
<contributor.author>Ko, KH</contributor.author>
<contributor.author>Baidoo, SE</contributor.author>
<contributor.author>Xu, H</contributor.author>
<contributor.author>Hua, Z</contributor.author>
<contributor.author>Lu, L</contributor.author>
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<subject.mesh>Arthritis, Experimental - etiology - pathology</subject.mesh>
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Author Affiliations
  1. Jiangsu University
  2. Nanjing University
  3. The University of Hong Kong