URSA小鼠模型中NKT细胞功能失调研究  

Dysfunction of NKT Cells in Murine Model of Unexplained Recurrent Spontaneous A bortion

作　　者：张勇[1] 王胜旺[1] 孙兵[2] 王福庆[1] 

机构地区：[1]上海第二医科大学上海市免疫学研究所,上海200025 [2]中国科学院上海生化与细胞学研究所,上海200031

出　　处：《上海免疫学杂志》2002年第6期383-387,共5页Shanghai Journal of Immunology

基　　金：国家自然科学基金资助项目 (No 3 0 0 70 70 9) ;中国科学院上海健康中心基金资助项目 ;上海市教委青年基金(No 2 0 0 0QN87)

摘　　要：利用原因不明复发性自发性流产 (URSA )小鼠模型 (CBA雌鼠×DBA/ 2J雄鼠 ) ,测定免疫性流产孕鼠不同孕期子宫蜕膜及胎盘内NKT细胞的数量及其分泌的细胞因子的格局 ,以调查NKT细胞数量和功能失调在URSA中的可能作用。研究结果显示 ,与正常孕鼠相比 ,流产模型鼠妊娠早期子宫和蜕膜中NKT细胞数量减少 ,分泌IFN γ能力降低。我们推测 ,妊娠早期子宫胎盘和蜕膜NKT细胞数量和功能失调可能是导致URSA的机制之一。In order to investigate the possible r ole of NKT cell dysfunction in the development of unexplained recurrent spontaneous abortion (URSA),we studied the quantity and cytokine profile of uterine and placental NKT cells in a URSA mouse model (female CBA mouse × male DBA/2J mouse) The results showed that the amount of uterine and placental NKT cells during the early stage of pregnancy was significantly decreased in the URSA mice as c ompared with that in the normal controls (female CBA × male CBA) In addition,IFN-γ levels produced by uterine and placental NKT cells of URSA mice were significantly reduced than those of normal NKT cells These results suggest that numerical and functional dysfunction of uterine and placental NKT cells during the early pregnancy might be a mechanism of URSA -

关 键 词：URSA 小鼠 NKT细胞 细胞因子 

分 类 号：R392.12[医药卫生—免疫学]