科研之友
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摘要
Objective: This study aims to explore the regulation of suppressor of cytokine signaling (SOCS1/ 3) on the differentiation of T cell and the role in Hashimoto's thyroiditis (HT). Methods: The CD4(+) T lymphocytes and B lymphocytes were separated from HT patients. The expression levels of SOCS1 and SOCS3 in CD4+ T cells were up-regulated using gene transfection technique, signal transducer and activator of transcription 3 (STAT3) was silenced simultaneously. They were co-cultured with B cells and their effects on the differentiation of TH17, Treg and Tfh cells were detected by flow cytometry. The CD4+ T cell related transcription factors such as retinoic acid related orphan receptor.t (ROR.t), Fork head box protein P3 (FOXP3) and B-cell lymphoma 6 (BCL 6) were detected by fluorescence quantitative PCR. The levels of cytokines in cell culture supernatant were detected by enzyme linked immunosorbent assay. The protein levels of SOCS3, SOCS1 and STAT3 were detected by western blotting method. Results: The expression of IL-17 was significantly reduced while the expression of Foxp3 was significantly increased after CD4+ T cells were transfected with SOCS1/3 and polarized in vitro for 72 h. Silencing stat3 inhibited the TH17 and Tfh cells while promoted Treg cells (P<0.01). SOCS1/3 and stat3 inhibited the ROR.t and BCL6 while promoted Foxp3. The inhibition of IL-6, L-17, IL-23 and IL-21 and the promotion of TGF-beta 1 were more obvious in SOCS1/3 + stat3 silence group than that of SOCS1/ 3 group and stat3 silence group (P<0.01). STAT3 protein levels significantly decreased and SOCS1/ 3 protein levels significantly increased in SOCS1/3 + stat3 silence group than that of control group (P<0.05). Conclusions: SOCS1/3 regulates the differentiation of T cells by inhibiting stat3, which may be related to the pathogenesis of HT.
- 出版日期2017
- 单位南昌大学
