摘要
目的:探讨妊娠17～37周正常和宫内感染时胎儿外周血可溶性白介素2受体(Soluble interleukin-2 receptor,sIL-2R)和自然杀伤细胞(Natural killer,NK)含量的变化.方法:超声引导下行脐带穿刺术,收集129例胎儿外周血,包括97例正常对照组胎儿血,32例宫内感染组(单纯疱疹病毒感染、弓形虫感染、风疹病毒感染)胎儿血,采用双色免疫荧光标记流式细胞仪技术测定胎儿外周血NK细胞百分率,双抗体夹心酶联免疫吸附试验测定胎儿外周血中sIL-2R的含量,分析生理状态下胎儿外周血NK细胞、sIL-2R的状况和宫内感染时NK细胞和sIL-2R含量的变化.结果:妊娠17～37周胎儿外周血NK细胞、sIL-2R含量不随孕周改变,r(NK)=-0.03,P＞0.05;r(sIL-2R)=0.167,P＞0.05,宫内感染时NK细胞含量减少,sIL-2R含量增多,与正常对照组相比差异有显著意义;t(NK)=4.29,P＜0.01;t(sIL-2R)=-5.833,P＜0.01.结论:妊娠17～37周胎儿外周血有一定量的NK细胞和sIL-2R存在,但机体免疫功能仍不完善,宫内感染时机体容易出现免疫抑制状态.
Objective： To investigate the contents of soluble interleukin-2 receptor（sIL-2R） and natural killer（NK） cell in nornal and infected fetuses during 17-37 gestational weeks. Methods： One hundred and twenty nine fetal blood samples were recruited by cordocentesis and among them, ninety seven were normal fetuses which were included in the control group. Thirty two were involved in the infective group which were infected by Herpes simplex virus,Toxoplasma gondii,or Rubella virus. NK cell was determined by two-colour fluorescence flow cytometry. sIL-2R level was determined by enzyme linked immuno-absorbent assay. Results： NK cell and sIL-2R level remained constant during 17 to 37 weeks＇ gestation： r （NK） = - 0.03, P 〉 0.05; r （sIL-2R） = 0.167, P 〉 0.05. Compared with the control group, the infected fetuses were characterized by a smaller percentage of NK cell and a high level of sIL-2R： t （NK） = 4.29, P 〈 0.01 ; t （slL-2R） = - 5.833, P 〈 0.01. Concludon：During 17 to 37 gestational weeks,there are some of NK cell and sIL-2R in fetal peripheral blood.The cell-mediated immunity of fetuses is not so strong that when in face of infection fetuses are easier to he immunosuppressive.
出处
《中国免疫学杂志》
CAS
CSCD
北大核心
2005年第10期768-771,共4页
Chinese Journal of Immunology
基金
广东省自然科学基金资助(031739)
关键词
胎儿
宫内感染
自然杀伤细胞
可溶性白介素2受体
Fetus
Intrauterine infection
Natural killer cell
Soluble interleukin-2 receptor
作者简介
杜涛（1977年-），女，硕士，住院医师，主要从事产前诊断和胎儿医学研究，现在中山大学附属第二医院工作；
指导教师及通讯作者：方群（1954年-），女，硕士，教授，硕士生导师，主要从事产前诊断和胎儿医学研究。mail：fang_qun@163．com。
