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目的:研究可溶性DC-SIGN(sDC-SIGN)对T细胞增殖及分泌细胞因子的影响。方法:无菌分离人外周血单个核细胞,免疫磁珠负选法分离纯化T细胞。以Con A、anti-CD3/anti-CD28单抗与sDC-SIGN共培养T细胞,流式细胞术检测CD4+、CD8+T细胞的增殖,ELISA检测培养上清中细胞因子的含量。结果:培养72 h时,对于Con A诱导的T细胞增殖,sDC-SIGN使CD4+、CD8+T细胞的增殖率分别由(11.42±0.20)%和(12.15±0.39)%下降到(2.61±0.05)%和(1.62±0.04)%(P<0.05);sDC-SIGN使Con A诱导T细胞配体上清中IL-2、IL-10、IFN-γ、IL-17A的含量(ng/L)分别由680.27±5.86、29.37±0.44、101.82±0.03、60.46±0.34下降到348.54±0.91、22.45±0.05、63.77±0.01、23.74±0.03(P<0.05),却使IL-6的含量(ng/L)由85.17±0.62增高到460.57±12.67(P<0.05)。对于anti-CD3/anti-CD28单抗诱导的T细胞增殖和细胞因子产生,sDC-SIGN也具有类似效应。此外,sDC-SIGN还下调Con A所刺激T细胞表达早期活化标志CD69。结论:sDC-SIGN可抑制T细胞增殖和影响细胞因子分泌,提示sDC-SIGN可能在T细胞介导免疫的调节中具有重要意义。
Objective: To study the effect of soluble DC-SIGN (sDC-SIGN) on the proliferation and secretion of cytokines in T cells. Methods: Peripheral blood mononuclear cells were isolated aseptically and immunomagnetic beads were used to isolate and purify T cells. T cells were co-cultured with Con A, anti-CD3 / anti-CD28 McAb and sDC-SIGN. The proliferation of CD4 + and CD8 + T cells was detected by flow cytometry. The contents of cytokines in the culture supernatants were detected by ELISA. Results: After 72 h of culture, sDC-SIGN decreased the proliferation rate of CD4 + and CD8 + T cells from (11.42 ± 0.20)% and (12.15 ± 0.39)% to (2.61 ± 0.05 ) And (1.62 ± 0.04)%, respectively (P <0.05). The levels of IL-2, IL-10, IFN-γ and IL-17A in Con A-induced T cell ligand supernatant ) Decreased from 680.27 ± 5.86,29.37 ± 0.44,101.82 ± 0.03,60.46 ± 0.34 to 348.54 ± 0.91,22.45 ± 0.05,63.77 ± 0.01,23.74 ± 0.03 respectively (P <0.05), but the content of IL-6 / L) increased from 85.17 ± 0.62 to 460.57 ± 12.67 (P <0.05). SDC-SIGN also has a similar effect on anti-CD3 / anti-CD28 mAb-induced T cell proliferation and cytokine production. In addition, sDC-SIGN also downregulated Con A-stimulated T cells to express early activation marker CD69. Conclusion: sDC-SIGN can inhibit T cell proliferation and affect cytokine secretion, suggesting that sDC-SIGN may play an important role in the regulation of T cell mediated immunity.