Invariant NKT cells increase lipopolysacchride-induced pregnancy loss by a mechanism involving Th1 and Th17 responses
Invariant NKT cells increase lipopolysacchride-induced pregnancy loss by a mechanism involving Th1 and Th17 responses
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不变的 NKT 细胞通过涉及 Th1 和 Th17 反应的机制增加脂多糖诱导的妊娠丢失
DOI：
10.3109/14767058.2013.773307
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发表时间：
2013-08-01
影响因子：
1.8
通讯作者：
Lin, Yi
中科院分区：
文献类型：
--
作者：
Li, Liping;Yang, Jing;Lin, Yi
目的：探讨不变性自然杀伤T细胞（iNKT）在感染相关性妊娠丢失中的作用。方法：对B6和iNKT细胞缺陷小鼠J α 18（-/-）腹腔注射脂多糖（LPS）或对照物，观察妊娠结局。分析iNKT细胞CD69的表达和细胞内细胞因子的产生。小鼠蜕膜iNKT细胞与LPS或pbs处理的树突状细胞（dc）共培养，并评估iNKT细胞CD69表达和细胞内和细胞外细胞因子的产生。结果：与B6小鼠相比，LPS处理的J α 18（-/-）小鼠在妊娠第6天和第9天的胚胎吸收率明显降低。与pbs处理的小鼠相比，在妊娠第6天或第9天注射LPS的B6小鼠的蜕膜iNKT细胞CD69表达和细胞内ifn - γ和IL-17的产生显著上调。与iNKT细胞和pbs处理的dc共培养相比，iNKT细胞和lps致敏dc共培养的上清液中ifn - γ和IL-17的水平显著增加。与与pbs处理的dc共培养的iNKT细胞相比，与lps致敏的dc共培养的iNKT细胞的CD69表达、细胞内ifn - γ和IL-17的产生显著上调。结论：iNKT细胞可能通过Th1和Th17细胞因子依赖的方式在lps诱导的妊娠丢失中发挥作用。
Objective: To determine the role of invariant natural killer T (iNKT) cells in infection-associated pregnancy loss.Methods: B6 and iNKT cell-deficient J alpha 18(-/-) mice were injected i.p. with lipopolysaccharide (LPS) or vehicle, and pregnancy outcomes were examined. Decidual iNKT cell expression of CD69 and intracellular cytokine production were analyzed. Mouse decidual iNKT cells were co-cultured with LPS or PBS-treated dendritic cells (DCs), and iNKT cell CD69 expression and intracellular and extracellular cytokine production were assessed.Results: The embryo resorption rate was notably lessened for J alpha 18(-/-) mice treated with LPS on day 6 or day 9 gestation in comparison with B6 mice treated with LPS. Decidual iNKT cell CD69 expression and intracellular IFN-gamma and IL-17 production for B6 mice injected with LPS on day 6 or day 9 gestation were significantly up-regulated compared with PBS-treated mice. Levels of IFN-gamma and IL-17 in the supernatants of the co-culture of decidual iNKT cells and LPS-sensitized DCs were strikingly increased in comparison with the co-culture of iNKT cells and PBS-treated DCs. CD69 expression and intracellular IFN-gamma and IL-17 production of iNKT cells co-cultured with LPS-sensitized DCs were remarkably up-regulated compared with iNKT cells co-cultured with PBS-treated DCs.Conclusions: Our results suggest that iNKT cells may play a role in LPS-induced pregnancy loss by Th1 and Th17 cytokine-dependent manner.