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Differentiation Imbalance of Th1/ Th17 in Peripheral Blood Mononuclear Cells Might Contribute to Pathogenesis of Hashimoto’s Thyroiditis
Author(s) -
Shi Y.,
Wang H.,
Su Z.,
Chen J.,
Xue Y.,
Wang S.,
Xue Y.,
He Z.,
Yang H.,
Zhou C.,
Kong F.,
Liu Y.,
Yang P.,
Lu L.,
Shao Q.,
Huang X.,
Xu H.
Publication year - 2010
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.2010.02425.x
Subject(s) - pathogenesis , peripheral blood mononuclear cell , thyroiditis , interferon gamma , immunology , retinoic acid , rar related orphan receptor gamma , cytokine , proinflammatory cytokine , biology , microbiology and biotechnology , endocrinology , immune system , inflammation , thyroid , foxp3 , in vitro , gene , biochemistry
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‐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.