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Article: Differentiation imbalance of Th1/Th17 in peripheral blood mononuclear cells might contribute to pathogenesis of Hashimoto's thyroiditis
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TitleDifferentiation imbalance of Th1/Th17 in peripheral blood mononuclear cells might contribute to pathogenesis of Hashimoto's thyroiditis
 
AuthorsShi, Y1
Wang, H1
Su, Z1
Chen, J1
Xue, Y1
Wang, S1
Xue, Y1
He, Z1
Yang, H1
Zhou, C1
Kong, F1
Liu, Y1
Yang, P1
Lu, L2
Shao, Q1
Huang, X1
Xu, H1
 
Issue Date2010
 
PublisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/SJI
 
CitationScandinavian Journal Of Immunology, 2010, v. 72 n. 3, p. 250-255 [How to Cite?]
DOI: http://dx.doi.org/10.1111/j.1365-3083.2010.02425.x
 
AbstractT helper 17(Th17) cell is a new subset of CD4+ T cells that produce a proinflammatory cytokine interleukin-17 (IL-17). Th17 cells have recently been shown to play a critical role in many autoimmune diseases that had previously been thought to be Th1 dominant. Although Hashimoto's thyroiditis (HT) was thought to be a Th1-type disease, the contributions of Th17 cells to the pathogenesis remain unclear. In this study, we investigated the expression levels of Th1/Th17 cell-associated factors in peripheral blood mononuclear cells (PBMC) and plasma from patients with HT by quantitative real-time polymerase chain reaction (RT-qPCR) and enzyme-linked immunosorbent assay (ELISA). Our results showed that the expression levels of Th1 cells-related T-bet and interferon-γ (IFN-γ) mRNA in PBMC from HT significantly decreased. However, the mRNA of Th17 coherent retinoic acid-related orphan nuclear receptor gamma t (RORγt) and IL-17 in patients with HT increased. In addition, a negative correlation between T-bet and RORγt mRNA expression was found in patients with HT, and the similar phenomena also appeared on the levels of mRNA and plasma concentration between IFN-γ and IL-17. It suggested that Th17 cells rather than Th1 cells predominated among patients suffering from HT, and Th17 cells might be involved in the pathogenesis of HT. © 2010 Blackwell Publishing Ltd.
 
ISSN0300-9475
2013 Impact Factor: 1.882
 
DOIhttp://dx.doi.org/10.1111/j.1365-3083.2010.02425.x
 
ISI Accession Number IDWOS:000280638800012
Funding AgencyGrant Number
National Natural Science Foundation of China30871193
30972748
Natural Science Foundation of Jiangsu Province Educational Commission09KJB310001
Innovation Fund for candidate of doctor in Jiangsu ProvinceCX09B_217Z
Health Department Foundation of Jiangsu ProvinceH200952
Funding Information:

This work was supported by the National Natural Science Foundation of China (Grant NO. 30871193, 30972748, respectively); Natural Science Foundation of Jiangsu Province Educational Commission (Grant No. 09KJB310001); Innovation Fund for candidate of doctor in Jiangsu Province (Grant NO. CX09B_217Z); Health Department Foundation of Jiangsu Province (Grant NO.H200952).

 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorShi, Y
 
dc.contributor.authorWang, H
 
dc.contributor.authorSu, Z
 
dc.contributor.authorChen, J
 
dc.contributor.authorXue, Y
 
dc.contributor.authorWang, S
 
dc.contributor.authorXue, Y
 
dc.contributor.authorHe, Z
 
dc.contributor.authorYang, H
 
dc.contributor.authorZhou, C
 
dc.contributor.authorKong, F
 
dc.contributor.authorLiu, Y
 
dc.contributor.authorYang, P
 
dc.contributor.authorLu, L
 
dc.contributor.authorShao, Q
 
dc.contributor.authorHuang, X
 
dc.contributor.authorXu, H
 
dc.date.accessioned2012-05-29T06:14:12Z
 
dc.date.available2012-05-29T06:14:12Z
 
dc.date.issued2010
 
dc.description.abstractT helper 17(Th17) cell is a new subset of CD4+ T cells that produce a proinflammatory cytokine interleukin-17 (IL-17). Th17 cells have recently been shown to play a critical role in many autoimmune diseases that had previously been thought to be Th1 dominant. Although Hashimoto's thyroiditis (HT) was thought to be a Th1-type disease, the contributions of Th17 cells to the pathogenesis remain unclear. In this study, we investigated the expression levels of Th1/Th17 cell-associated factors in peripheral blood mononuclear cells (PBMC) and plasma from patients with HT by quantitative real-time polymerase chain reaction (RT-qPCR) and enzyme-linked immunosorbent assay (ELISA). Our results showed that the expression levels of Th1 cells-related T-bet and interferon-γ (IFN-γ) mRNA in PBMC from HT significantly decreased. However, the mRNA of Th17 coherent retinoic acid-related orphan nuclear receptor gamma t (RORγt) and IL-17 in patients with HT increased. In addition, a negative correlation between T-bet and RORγt mRNA expression was found in patients with HT, and the similar phenomena also appeared on the levels of mRNA and plasma concentration between IFN-γ and IL-17. It suggested that Th17 cells rather than Th1 cells predominated among patients suffering from HT, and Th17 cells might be involved in the pathogenesis of HT. © 2010 Blackwell Publishing Ltd.
 
dc.description.natureLink_to_subscribed_fulltext
 
dc.identifier.citationScandinavian Journal Of Immunology, 2010, v. 72 n. 3, p. 250-255 [How to Cite?]
DOI: http://dx.doi.org/10.1111/j.1365-3083.2010.02425.x
 
dc.identifier.citeulike7616476
 
dc.identifier.doihttp://dx.doi.org/10.1111/j.1365-3083.2010.02425.x
 
dc.identifier.epage255
 
dc.identifier.hkuros176946
 
dc.identifier.isiWOS:000280638800012
Funding AgencyGrant Number
National Natural Science Foundation of China30871193
30972748
Natural Science Foundation of Jiangsu Province Educational Commission09KJB310001
Innovation Fund for candidate of doctor in Jiangsu ProvinceCX09B_217Z
Health Department Foundation of Jiangsu ProvinceH200952
Funding Information:

This work was supported by the National Natural Science Foundation of China (Grant NO. 30871193, 30972748, respectively); Natural Science Foundation of Jiangsu Province Educational Commission (Grant No. 09KJB310001); Innovation Fund for candidate of doctor in Jiangsu Province (Grant NO. CX09B_217Z); Health Department Foundation of Jiangsu Province (Grant NO.H200952).

 
dc.identifier.issn0300-9475
2013 Impact Factor: 1.882
 
dc.identifier.issue3
 
dc.identifier.pmid20696023
 
dc.identifier.scopuseid_2-s2.0-77955298749
 
dc.identifier.spage250
 
dc.identifier.urihttp://hdl.handle.net/10722/148626
 
dc.identifier.volume72
 
dc.languageeng
 
dc.publisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/SJI
 
dc.publisher.placeUnited Kingdom
 
dc.relation.ispartofScandinavian Journal of Immunology
 
dc.relation.referencesReferences in Scopus
 
dc.subject.meshAdult
 
dc.subject.meshCell Differentiation - Immunology
 
dc.subject.meshFemale
 
dc.subject.meshGene Expression - Genetics
 
dc.subject.meshHashimoto Disease - Blood - Etiology - Immunology - Pathology
 
dc.subject.meshHumans
 
dc.subject.meshInterferon-Gamma - Blood - Genetics
 
dc.subject.meshInterleukin-17 - Blood - Genetics - Metabolism
 
dc.subject.meshInterleukin-23 Subunit P19 - Blood - Genetics
 
dc.subject.meshInterleukin-6 - Blood - Genetics
 
dc.subject.meshLeukocytes, Mononuclear - Cytology - Immunology - Metabolism
 
dc.subject.meshMale
 
dc.subject.meshMiddle Aged
 
dc.subject.meshNuclear Receptor Subfamily 1, Group F, Member 3 - Genetics
 
dc.subject.meshT-Box Domain Proteins - Genetics
 
dc.subject.meshT-Lymphocytes, Helper-Inducer - Cytology - Immunology - Metabolism - Pathology
 
dc.subject.meshTh1 Cells - Cytology - Immunology - Metabolism - Pathology
 
dc.subject.meshYoung Adult
 
dc.titleDifferentiation imbalance of Th1/Th17 in peripheral blood mononuclear cells might contribute to pathogenesis of Hashimoto's thyroiditis
 
dc.typeArticle
 
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Author Affiliations
  1. Jiangsu University
  2. The University of Hong Kong