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目的:研究TGF-β1对树突状细胞(DC)的分化、成熟及功能影响。方法:应用100万U/L粒-巨噬细胞集落刺激因子(GM-CSF)和白细胞介素-4(IL-4)7d诱导单核细胞分化为不成熟DC,加入终浓度20万U/L的肿瘤坏死因子-α(TNF-α)48h后获得成熟DC的体外模型,将TGF-β1加入该模型中,用流式细胞术分别检测DC分化,成熟阶段细胞表型的变化,应用ELISA检测DCIL-12的分泌水平,应用MTT法检测DC刺激同种异体T细胞增殖的能力。结果:TGF-β1对不成熟DC的特征性分子CD1a的表达无明显影响,但在诱导DC的成熟阶段,TGF-β1明显抑制CD40、CD86及CD83上调。此外,TGF-β1显著减少DCIL-12的分泌,显著抑制DC刺激同种异体T细胞增殖的能力。结论:DC是TGF-β1免疫抑制活性的靶细胞。TGF-β1不影响DC的分化,但抑制DC的成熟和细胞因子的分泌,降低DC刺激同种异体反应T细胞增殖的能力。
Objective: To study the effect of TGF-β1 on differentiation, maturation and function of dendritic cells (DCs). Methods: Monocytes were induced to differentiate into immature DCs with 1 million U / L granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin-4 (IL-4) L (TNF-α) for 48h, the mature DCs were obtained in vitro and TGF-β1 was added into the model. The changes of cell phenotypes in DC differentiation and maturation stages were detected by flow cytometry. The level of DCIL-12 secretion was detected. The ability of DC to stimulate the proliferation of allogeneic T cells was detected by MTT assay. Results: TGF-β1 had no significant effect on the expression of CD1a, a characteristic molecule of immature DC. However, TGF-β1 significantly inhibited the up-regulation of CD40, CD86 and CD83 during the induction of DC maturation. In addition, TGF-β1 significantly reduced the secretion of DCIL-12 and markedly inhibited the ability of DCs to stimulate the proliferation of allogeneic T cells. Conclusion: DC is the target cell of immunosuppressive activity of TGF-β1. TGF-β1 does not affect the differentiation of DC, but inhibits the maturation of DC and the secretion of cytokines, and decreases the ability of DC to stimulate the proliferation of alloreactive T cells.