title: Differentiation imbalance of Th1/Th17 in peripheral blood mononuclear cells might contribute to pathogenesis of Hashimoto's thyroiditis.
abstract: T 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-gamma (IFN-gamma) mRNA in PBMC from HT significantly decreased. However, the mRNA of Th17 coherent retinoic acid-related orphan nuclear receptor gamma t (RORgammat) and IL-17 in patients with HT increased. In addition, a negative correlation between T-bet and RORgammat mRNA expression was found in patients with HT, and the similar phenomena also appeared on the levels of mRNA and plasma concentration between IFN-gamma 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.
authors.affiliation: Department of Immunology and Laboratory Immunology, Institute of Laboratory Medicine, Jiangsu University, Zhenjiang, China.
authors.forename: Y
authors.initials: Y
authors.lastname: Shi
authors.forename: H
authors.initials: H
authors.lastname: Wang
authors.forename: Z
authors.initials: Z
authors.lastname: Su
authors.forename: J
authors.initials: J
authors.lastname: Chen
authors.forename: Y
authors.initials: Y
authors.lastname: Xue
authors.forename: S
authors.initials: S
authors.lastname: Wang
authors.forename: Y
authors.initials: Y
authors.lastname: Xue
authors.forename: Z
authors.initials: Z
authors.lastname: He
authors.forename: H
authors.initials: H
authors.lastname: Yang
authors.forename: C
authors.initials: C
authors.lastname: Zhou
authors.forename: F
authors.initials: F
authors.lastname: Kong
authors.forename: Y
authors.initials: Y
authors.lastname: Liu
authors.forename: P
authors.initials: P
authors.lastname: Yang
authors.forename: L
authors.initials: L
authors.lastname: Lu
authors.forename: Q
authors.initials: Q
authors.lastname: Shao
authors.forename: X
authors.initials: X
authors.lastname: Huang
authors.forename: H
authors.initials: H
authors.lastname: Xu
mesh_terms: D000328:Adult; D002454:Cell Differentiation / Q000276:immunology*; D005260:Female; D015870:Gene Expression / Q000235:genetics; D050031:Hashimoto Disease / Q000097:blood / Q000209:etiology / Q000276:immunology* / Q000473:pathology*; D006801:Humans; D007371:Interferon-gamma / Q000097:blood / Q000235:genetics; D020381:Interleukin-17 / Q000097:blood / Q000235:genetics / Q000378:metabolism*; D053760:Interleukin-23 Subunit p19 / Q000097:blood / Q000235:genetics; D015850:Interleukin-6 / Q000097:blood / Q000235:genetics; D007963:Leukocytes, Mononuclear / Q000166:cytology* / Q000276:immunology / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D057132:Nuclear Receptor Subfamily 1, Group F, Member 3 / Q000235:genetics; D020825:T-Box Domain Proteins / Q000235:genetics; D006377:T-Lymphocytes, Helper-Inducer / Q000166:cytology* / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D018417:Th1 Cells / Q000166:cytology* / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D055815:Young Adult; D000098815:T-bet Transcription Factor
chemical_list: D020381:Interleukin-17; D053760:Interleukin-23 Subunit p19; D015850:Interleukin-6; D057132:Nuclear Receptor Subfamily 1, Group F, Member 3; D020825:T-Box Domain Proteins; D000098815:T-bet Transcription Factor; D007371:Interferon-gamma