摘要
背景:巨噬细胞迁移抑制因子(MIF)是一种免疫调节性细胞因子,作为先天性和适应性免疫反应的调节因子起着至关重要的作用,通过促进血管生成和诱导促炎细胞因子和基质金属蛋白参与类风湿关节炎(RA)关节的破坏过程。SES(MMP)。我们评估了重组人MIF(rhmif)是否诱导RA患者和对照组(cs)外周血单个核细胞(pbmc)中TNF-α、IFN-γ、IL-1β、IL-6、IL-10、IL-17a和IL-17f的产生。 方法:采用LPS、rhmif或MIF拮抗剂iso-1联合刺激RA患者和CS患者的PBMC 24小时。细胞因子谱用多重免疫分析法测定,巨噬细胞迁移抑制因子(MIF)用酶联免疫吸附测定试剂盒测定。 结果:在rhmif刺激下,CS和RA的PBMC产生Th1和Th17细胞因子,但在RA患者的细胞中这种作用更明显。与未受刺激的细胞相比,来自RA患者的rhmifs刺激的PBMC产生更高水平的Th1和Th17细胞因子:TNF-α(538.81 vs.5.02 pg/ml,p<0.001)、IFN-γ(721.90 vs.8.40 pg/ml,p<0.001)、IL-1β(150.14 vs.5.17 pg/ml,p<0.05,p<0.15 pg/ml,150.14 vs.5.17 pg/ml,p<0.05)、IL-6(19769.70 vs.119.85 pg/ml,19769.70 vs.119.70 p19.85 pg/ml,p<0.001,p<0.001,p<0.001,p<119.70.70 p和IL-17F(158.43对0.92 pg/ml,p<0.001)。 结论:这些结果突出了MIF在通过Th1和Th17细胞因子谱诱导的RA慢性炎症过程中的潜在作用,为MIF刺激RA和CS PBMC中IL-17a和IL-17f表达提供了新的证据。
关键词: MIF,抗菌药物可调节Th1 th17,型材,型材,外周血单个核细胞,类风湿性关节炎。
Current Molecular Medicine
Title:Th1/Th17 Cytokine Profile is Induced by Macrophage Migration Inhibitory Factor in Peripheral Blood Mononuclear Cells from Rheumatoid Arthritis Patients
Volume: 18 Issue: 10
关键词: MIF,抗菌药物可调节Th1 th17,型材,型材,外周血单个核细胞,类风湿性关节炎。
摘要: Background: Macrophage migration inhibitory factor (MIF) is an immunoregulatory cytokine that plays a crucial role as a regulator of the innate and adaptive immune responses and takes part in the destructive process of the joint in rheumatoid arthritis (RA) by promoting angiogenesis and inducing proinflammatory cytokines and matrix metalloproteinases (MMP). We evaluated if recombinant human MIF (rhMIF) induces the production of TNF-α, IFN-γ, IL-1β, IL-6, IL-10, IL-17A, and IL- 17F in peripheral blood mononuclear cells (PBMC) from RA patients and control subjects (CS).
Methods: The PBMC from RA patients and CS were stimulated for 24 hours with combinations of LPS, rhMIF or the MIF antagonist ISO-1. Cytokine profiles were measured using a multiplex immunoassay and, macrophage migration inhibitory factor (MIF) was determined by ELISA kit.
Results: The PBMC of CS and RA produced Th1 and Th17 cytokines under stimulation with rhMIF, however, this effect was higher in the cells of RA patients. The rhMIFstimulated PBMC from RA patients produced higher levels of Th1 and Th17 cytokines in comparison with unstimulated cells: TNF-α (538.81 vs. 5.02 pg/mL, p<0.001), IFN-γ (721.90 vs. 8.40 pg/mL, p<0.001), IL-1β (150.14 vs. 5.17 pg/mL, p<0.05), IL-6 (19769.70 vs. 119.85 pg/mL, p<0.001), IL-17A (34.97 vs. 0.90 pg/mL, p<0.01) and IL-17F (158.43 vs. 0.92 pg/mL, p<0.001).
Conclusion: These results highlight the potential role of MIF in the establishment of the chronic inflammatory process in RA via Th1 and Th17 cytokine profile induction and provide new evidence of the role of MIF to stimulate the IL-17A and IL-17F expression in PBMC from RA and CS.
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Cite this article as:
Th1/Th17 Cytokine Profile is Induced by Macrophage Migration Inhibitory Factor in Peripheral Blood Mononuclear Cells from Rheumatoid Arthritis Patients, Current Molecular Medicine 2018; 18 (10) . https://dx.doi.org/10.2174/1566524019666190129123240
DOI https://dx.doi.org/10.2174/1566524019666190129123240 |
Print ISSN 1566-5240 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5666 |
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