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  • 标题:Evaluation of Th1/Th2 Lymphocyte Balance in Peripheral Blood Mononuclear Cells of Patients with Hashimoto’s Thyroiditis
  • 本地全文:下载
  • 作者:Hajar VASEGHI ; Fatemeh ESFAHANIAN ; Zohreh JADALI
  • 期刊名称:Iranian Journal of Public Health
  • 印刷版ISSN:2251-6085
  • 电子版ISSN:2251-6093
  • 出版年度:2020
  • 卷号:49
  • 期号:3
  • DOI:10.18502/ijph.v49i3.3152
  • 语种:English
  • 出版社:Tehran University of Medical Sciences
  • 摘要:Background: The role of T cells in the pathogenesis of Hashimoto’s thyroiditis is well established, whereas the precise and likely the overlapping contributions of different T-cell subpopulations to thyroid injury are less understood. The purpose of this study was to assess the expression pattern of two lineage determining transcription factors, T-bet and GATA-3 that regulate differentiation of T cells into Th1 or Th2 cell fates, respectively. Moreover, the mRNA expression and plasma concentration of Th1(IFN-γ) and Th2(IL-4) cytokineswere analyzed. Methods: In this case-control study, reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was performed to determine the expression patterns of various transcripts in 20 patients (in Endocrinology Clinic, Imam Khomeini Hospital Complex, Tehran University of Medical Sciences, Tehran, Iran, in 2015) with Hashimoto’s thyroiditis (HT) and 22 healthy controls. Plasma IL-4 and IFN-γ concentrations were also measured using enzyme-linked immunosorbent assay. Results: T-bet gene expression was significantly lower in patients compared to healthy controls (P=0.014). The expression of IL-4 mRNAs was significantly increased in the  peripheral blood mononuclear cells from patients as compared to normal controls (P=0.001). In addition, a marked increase in plasma IL-4 levels were observed in patient group compared to controls (P=0.043). Conclusion: Altered balance between Th1 and Th2 related transcription factors and cytokines may be implicated in the pathogenesis of Hashimoto’s thyroiditis.
  • 关键词:Hashimoto's thyroiditis; T lymphocyte; Autoimmunity; Cytokine
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