吲哚胺2,3-双加氧酶及IL-12/IL-10细胞因子平衡与妊娠免疫耐受

Association of indoleamine 2,3-dioxygenase and IL-12/IL-10 balance with pregnant tolerance

目的 :观察妊娠不同时期胎盘来源的单核-巨噬细胞吲哚胺2,3-双加氧酶(indoleamine 2,3-dioxygenase,IDO)的表达及细胞因子白细胞介素(IL)-10、IL-12的分泌情况,探讨其在妊娠免疫耐受中的可能作用。方法:机械分离中期妊娠(21周±3天,19例)及足月妊娠(39周±5天,25例)胎盘中的单核-巨噬细胞,ELISA法检测其分泌IL-10、IL-12的水平;RT-PCR及Western blot法分别检测IDO mRNA及蛋白水平的表达;以CCK-8法检测其激发同种异体T细胞增殖能力的不同。结果:足月妊娠较中期妊娠胎盘来源的单核-巨噬细胞产生更多的IL-12,但IL-10及IDO的表达较之明显减低;并且,足月妊娠较中期妊娠胎盘来源的单核-巨噬细胞刺激同种异体淋巴细胞增殖的能力更强。结论:中期及足月妊娠胎盘来源的单核-巨噬细胞参与维持妊娠免疫耐受及分娩发动可能与其调节IL-12/IL-10细胞因子平衡及影响IDO的表达有关,但IL-12/IL-10细胞因子平衡与单核-巨噬细胞IDO表达的关系还有待进一步研究。

Objective：To estimate the possible effect of placental monocyte-macrophages on the pregnant immunological tolerance by observing the expression of indoleamine 2,3-dioxygenase （IDO） and the secretion of IL-10 and IL-12 in cells from different gestational phages. Methods： Monocyte-macrophages cells were separated mechanically from normal term （39 weeks ＋ 5 days, 25 cases） and midtrimester （21 weeks ± 3 days, 19 cases） placental tissues. The cytokines including IL-12 and IL-10 were assayed by ELISA,while the expression of IDO was measured by RT-PCR and Western blot,respectively. The monocyte-macrophages ceils derived from placental tissue in different gestational phages were co-cultured with allogeneic T cells in order to detect their abilities in stimulating the proliferation of allogeneic T cells detected by CCK-8. Results： Monocyte-macrophages cells from normal term placental tissues secreted high level of IL-12,but expressed low levels of IL-10 and IDO. Besides,monocyte-macrophages cells from normal term placental tissues were more powerful in promoting the proliferation of allogeneic T cells than the ceils from midtrimester term placental tissues. Conclusion： Monocyte-macrophages cells from normal term and midtrimester placental tissues may play roles in the maintenance of pregnant immunological tolerance and delivery possibly by placental tissue in different gestational phages possess different biological characters,which possibly by regulating the IL-12/IL-10 balance and IDO expression. However, the association of IL-12/IL-10 balance with the expression of IDO needs further elucidation.