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作 者:李莉平[1] 杨静[1] 杨宇[1] 任丽华[1] 康佳丽[1]
机构地区:[1]广州医学院附属广州市第一人民医院妇产科,510180
出 处:《免疫学杂志》2013年第2期126-129,共4页Immunological Journal
基 金:国家自然科学基金(81200478);广东省医学科研基金项目(A2012493);广州市医药卫生科技项目(20121A011020)
摘 要:目的探讨恒定自然杀伤T(iNKT)细胞在脂多糖(LPS)诱导的早产中的作用。方法野生型C56BL/6小鼠和缺乏iNKT细胞的Jα18-/-小鼠腹腔注射LPS建立炎症诱导性早产小鼠模型;计算早产率和死胎率;流式细胞术检测蜕膜活化型免疫细胞百分率和树突状细胞共刺激分子的表达。结果与野生型小鼠比较,LPS处理的Jα18-/-小鼠早产率和死胎率显著降低,蜕膜树突状细胞共刺激分子CD40、CD80和CD86的表达显著下降,蜕膜活化型树突状细胞、T细胞和NK细胞百分率明显减少。结论 iNKT细胞可能在LPS诱导的早产发生中具有重要作用。The aim of the study was to investigate the roles of invariant natural killer T(iNKT) cells in lipopolysaccharide(LPS)-induced preterm delivery.Firstly,wild-type(WT) C57BL/6 mice and iNKT cell-deficient Jα18-/-mice were injected intraperitoneally with LPS to establish a murine model of inflammation-induced preterm delivery.Then we analyzed the expression of costimulatory molecules on decidual dendritic cells,and the percentages of decidual activated immune cells by flow cytometry.Results demonstrated that the rates of preterm delivery and fetal death were markedly reduced in LPS-treated Jα18-/-mice in comparison with LPS-treated WT mice;the CD40,CD80 and CD86 expression levels on decidual CD11c+ cells from Jα18-/-mice were strikingly lessened compared with WT mice;the percentages of activated decidual dendritic cells,T cells and NK cells were significantly lower in Jα18-/-mice than in WT mice.Our results suggested that iNKT cells may play an important role in LPS-induced preterm delivery.
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