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目的 :研究IL 1 0对单核细胞来源的DC体外发育分化和功能的影响及TNF α和sCD4 0L对IL 1 0抑制DC生物学功能的阻断或逆转效应。方法 :检测经IL 1 0抑制及添加上述干预因素后DC的表型、刺激T细胞增殖和分泌IL 1 2的能力。结果 :IL 1 0能够抑制幼稚DC的成熟 ,促进其向巨噬细胞分化 ,并伴随有DC激发T细胞增殖和分泌IL 1 2能力明显下降 ,这种抑制效应与IL 1 0浓度存在相关性 ;IL 1 0对由sCD4 0L诱导成熟的DC无抑制作用 ,但能抑制TNF α诱导成熟DC分泌IL 1 2的能力 ;在IL 1 0作用后加入TNF α或sCD4 0L均不能逆转IL 1 0对DC抑制作用 ;在IL 1 0作用的同时加入sCD4 0L而不是TNF α ,能完全阻断IL 1 0抑制DC刺激T细胞增殖和分泌IL 1 2的作用。结论 :IL 1 0是肿瘤细胞逃脱免疫攻击的重要因子 ,能够抑制DC的成熟、抗原提呈以及削弱其刺激T细胞增殖的能力等多重负性作用 ,其对由TNF α或sCD4 0L途径诱导成熟的DC的抑制作用不一致 ,CD4 0信号干预对制备肿瘤免疫治疗运用的DC具有重要的价值
OBJECTIVE: To investigate the effect of IL-10 on monocyte-derived DCs in vitro and to investigate the role of TNFα and sCD40L in blocking or reversing the biological function of IL-10-induced DCs. Methods: The phenotypes of DCs after IL-10 inhibition and addition of these intervention factors were assayed to stimulate T cell proliferation and secretion of IL-12. Results: IL 1 0 could inhibit the maturation of naive DCs and promote their differentiation into macrophages, accompanied by a significant decrease of T cell proliferation and IL 1 2 secretion induced by DC. This inhibitory effect was correlated with the concentration of IL 1 0. IL10 did not inhibit the maturation of DCs induced by sCD40L, but inhibited the ability of TNFa to induce the secretion of IL-12 by mature DCs. The addition of either TNFa or sCD40L did not reverse the effect of IL10 on DCs Inhibition of IL-10 by addition of sCD40L instead of TNFα completely blocked the effect of IL-10 on DC-stimulated T cell proliferation and IL-2 secretion. CONCLUSION: IL-10 is an important factor in escaping immune attack of tumor cells, and can inhibit the maturation of DCs, antigen presentation and the ability of stimulating T cell proliferation. IL-10 induces maturation induced by TNFα or sCD40L Of DC inhibitory effect is inconsistent, CD4 0 signal intervention for the preparation of tumor immunotherapy with DC has important value