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目的:探讨外周血单个核细胞(PBMCs)经CD3、CD28双信号通路活化后白细胞介素17A(IL-17A)的分泌以及免疫调节剂雷公藤甲素对该细胞因子分泌的影响。方法:抗CD3单克隆抗体(浓度10μg/ml)和抗CD28单克隆抗体(浓度5μg/ml)共刺激PBMCs,模拟T细胞在体内受双信号免疫活化的过程,应用酶联免疫吸附方法(ELISA)检测细胞培养液上清IL-17A水平。结果:外周血单个核细胞经CD3/CD28双信号通路刺激后,其分泌的IL-17A在6h内即出现明显增加,并在24h内呈继续增高的趋势;100nmol/L和500nmol/L浓度的雷公藤甲素均能够显著抑制该细胞分泌IL-17A。结论:PBMCs经双信号免疫活化后,其分泌的IL-17A明显增加,可能是哮喘气道变应性炎症的形成和发展机制之一;雷公藤甲素能够通过抑制PBMCs对IL-17A分泌,从而有可能减轻哮喘气道炎症。
Objective: To investigate the secretion of interleukin 17A (IL-17A) after activation of peripheral blood mononuclear cells (PBMCs) by CD3 and CD28 dual signal pathways and the effect of immunomodulator triptolide on cytokine secretion. METHODS: PBMCs were co-stimulated with anti-CD3 monoclonal antibody (concentration: 10 μg/ml) and anti-CD28 monoclonal antibody (concentration: 5 μg/ml). The imitation of T-cells was stimulated by dual signal in vivo. The enzyme-linked immunosorbent assay (ELISA) was used. ) The supernatant of the cell culture supernatant was assayed for IL-17A levels. RESULTS: After stimulated by CD3/CD28 dual signal pathway, peripheral blood mononuclear cells secreted IL-17A within 6 hours and increased continuously within 24 hours. The concentration of 100nmol/L and 500nmol/L increased. Triptolide can significantly inhibit the secretion of IL-17A by this cell. Conclusion: The IL-17A secreted by PBMCs after two-signal immunization was significantly increased, which may be one of the mechanisms of asthma allergic inflammation. Triptolide can inhibit the secretion of IL-17A by inhibiting PBMCs. Thus it is possible to reduce airway inflammation in asthma.