Yao Qiu-Ming, Li Ling, Song Zhen-Yu, Wang Bin, Qin Qiu, An Xiao-Fei, Zhang Jin-An
Department of Endocrinology, Jinshan Hospital of Fudan University, Shanghai, China.
Department of Urology, Jinshan Hospital of Fudan University, Shanghai, China.
Front Endocrinol (Lausanne). 2018 Oct 9;9:591. doi: 10.3389/fendo.2018.00591. eCollection 2018.
IL-36α is involved in the pathogenesis of a variety of autoimmune diseases, but the relationship between IL-36α and Graves' disease (GD) has rarely investigated. In the present study, we aimed to explore the expression of IL-36α and elucidate the potential role of IL-36α in GD. The expression of IL-36α mRNA in peripheral blood mononuclear cells (PBMCs) from 32 newly diagnosed GD patients, 15 refractory GD patients and 30 normal controls (NC) was examined using quantitative real-time polymerase chain reaction (qRT-PCR). The level of IL-36α in serum from 46 newly diagnosed GD patients, 10 refractory GD patients and 24 NC was measured using enzyme linked immunosorbent assay (ELISA). The percentage of CD4IL-36αT cells was detected by flow cytometry. PBMCs from newly diagnosed GD patients and NC group were cultured in the presence or absence of recombinant human IL-36α, and the expression levels of IFN-γ, TNF-α, IL-6, and IL-17A in culture supernatant were detected by cytokine array. The expression of IL-36α mRNA in newly diagnosed GD patients was significantly higher than that in NC group ( = 0.019). IL-36α mRNA expression was positively associated with thyrotropin receptor antibody (TRAb) ( = 0.004, = 0.498) in newly diagnosed GD patients. The level of IL-36α in serum from newly diagnosed GD patients was significantly higher than that in refractory GD patients and NC group ( = 0.01; = 0.007). The percentage of CD4IL-36αT cells in newly diagnosed GD patients was significantly higher than that in NC group ( = 0.030). In GD group, recombinant human IL-36α stimulation resulted in the increase of INF-γ, TNF-α, IL-6 and IL-17A ( = 0.015; = 0.016; = 0.039; = 0.017). IL-36α and CD4IL-36αT cells may be involved in the pathogenesis of GD by promoting the production of Th1, Th2, and Th17 cytokines.
白细胞介素-36α（IL-36α）参与多种自身免疫性疾病的发病机制，但IL-36α与格雷夫斯病（GD）之间的关系鲜有研究。在本研究中，我们旨在探讨IL-36α的表达情况，并阐明IL-36α在GD中的潜在作用。采用定量实时聚合酶链反应（qRT-PCR）检测32例新诊断的GD患者、15例难治性GD患者和30例正常对照（NC）外周血单个核细胞（PBMC）中IL-36α mRNA的表达。采用酶联免疫吸附测定（ELISA）检测46例新诊断的GD患者、10例难治性GD患者和24例NC血清中IL-36α的水平。通过流式细胞术检测CD4IL-36αT细胞的百分比。将新诊断的GD患者和NC组的PBMC在有或无重组人IL-36α的情况下培养，通过细胞因子芯片检测培养上清中IFN-γ、TNF-α、IL-6和IL-17A的表达水平。新诊断的GD患者中IL-36α mRNA的表达显著高于NC组（ = 0.019）。新诊断的GD患者中IL-36α mRNA表达与促甲状腺素受体抗体（TRAb）呈正相关（ = 0.004， = 0.498）。新诊断的GD患者血清中IL-36α水平显著高于难治性GD患者和NC组（ = 0.01； = 0.007）。新诊断的GD患者中CD4IL-36αT细胞的百分比显著高于NC组（ = 0.030）。在GD组中，重组人IL-36α刺激导致INF-γ、TNF-α、IL-6和IL-17A增加（ = 0.015； = 0.016； = 0.039； = 0.017）。IL-36α和CD4IL-36αT细胞可能通过促进Th1、Th2和Th17细胞因子的产生参与GD的发病机制。
Zotero 插件
