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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

TitleGlucocorticoid-induced tumor necrosis factor receptor family-related protein exacerbates collagen-induced arthritis by enhancing the expansion of Th17 cells
Authors
Issue Date2012
PublisherElsevier Inc.. The Journal's web site is located at http://ajp.amjpathol.org/
Citation
The American Journal of Pathology: cellular and molecular biology of disease, 2012, v. 180 n. 3, p. 1059-1067 How to Cite?
Abstract
Rheumatoid 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.
Persistent Identifierhttp://hdl.handle.net/10722/164840
ISSN
2013 Impact Factor: 4.602
ISI Accession Number ID

 

Author Affiliations
  1. Jiangsu University
  2. Nanjing University
  3. The University of Hong Kong
DC FieldValueLanguage
dc.contributor.authorWang, Sen_US
dc.contributor.authorShi, Yen_US
dc.contributor.authorYang, Men_US
dc.contributor.authorMa, Jen_US
dc.contributor.authorTian, Jen_US
dc.contributor.authorChen, Jen_US
dc.contributor.authorMao, Cen_US
dc.contributor.authorJiao, Zen_US
dc.contributor.authorKo, KHen_US
dc.contributor.authorBaidoo, SEen_US
dc.contributor.authorXu, Hen_US
dc.contributor.authorHua, Zen_US
dc.contributor.authorLu, Len_US
dc.date.accessioned2012-09-20T08:10:43Z-
dc.date.available2012-09-20T08:10:43Z-
dc.date.issued2012en_US
dc.identifier.citationThe American Journal of Pathology: cellular and molecular biology of disease, 2012, v. 180 n. 3, p. 1059-1067en_US
dc.identifier.issn0002-9440en_US
dc.identifier.urihttp://hdl.handle.net/10722/164840-
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.languageengen_US
dc.publisherElsevier Inc.. The Journal's web site is located at http://ajp.amjpathol.org/-
dc.relation.ispartofThe American Journal of Pathology: cellular and molecular biology of diseaseen_US
dc.rightsNOTICE: this is the author’s version of a work that was accepted for publication in <Journal title>. 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 cellsen_US
dc.typeArticleen_US
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1525-2191 (Electronic) 0002-9440 (Linkin&volume=180&issue=3&spage=1059&epage=67&date=2012&atitle=Glucocorticoid-induced+tumor+necrosis+factor+receptor+family-related+protein+exacerbates+collagen-induced+arthritis+by+enhancing+the+expansion+of+Th17+cellsen_US
dc.identifier.emailWang, S: sjwjs@ujs.edu.cnen_US
dc.identifier.emailKo, KH: khko@hkucc.hku.hken_US
dc.identifier.emailLu, L: liweilu@hkucc.hku.hk-
dc.identifier.authorityLu, L=rp00477en_US
dc.identifier.doi10.1016/j.ajpath.2011.11.018-
dc.identifier.pmid22214837-
dc.identifier.scopuseid_2-s2.0-84863171449-
dc.identifier.hkuros208155en_US
dc.identifier.volume180en_US
dc.identifier.issue3en_US
dc.identifier.spage1059en_US
dc.identifier.epage1067en_US
dc.identifier.isiWOS:000301022200019-
dc.publisher.placeUnited States-
dc.identifier.citeulike10625413-

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