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作 者:金莉萍[1] 李大金[1] 王明雁[1] 朱影[1] 袁敏敏[1] 孟毅[1]
机构地区:[1]复旦大学附属妇产科研究所生殖免疫研究室,上海200011
出 处:《中华微生物学和免疫学杂志》2004年第12期932-935,共4页Chinese Journal of Microbiology and Immunology
基 金:国家自然科学基金(39770773);复旦大学"985工程"项目(985B36);计划生育药具国家重点实验室课题(B2021)资助项目
摘 要:目的探讨过继转输胚胎抗原耐受性T、B细胞对宿主孕鼠妊娠预后及母胎界面TH1TH2型细胞因子表达的影响。方法♀CBAJ×♂DBA2为自然流产模型,于孕4d(着床期)分别腹腔注射大鼠抗小鼠CD80和CD86McAb或大鼠同型IgG。于孕9d,分选脾脏T细胞和B细胞,并过继转输至孕4d的自然流产模型♀CBAJ×♂DBA2孕鼠,孕第14天测定宿主母胎界面组织体外培养上清液中TH1TH2型细胞因子(IL4、IL10、TNFα、IFNγ)水平,并比较各组宿主孕鼠胚胎吸收率。结果转输胚胎抗原耐受T细胞和转输正常妊娠模型孕鼠的T细胞均使宿主孕鼠母胎界面IL4和IL10表达显著增加,而IFNγ和TNFα表达则显著下降,且胚胎吸收率也显著下降(P<0.05)。结论于孕早期过继转输胚胎抗原耐受T细胞和正常妊娠模型孕鼠的T细胞可通过调节宿主孕鼠母胎界面TH1TH2型细胞因子的平衡,从而诱导母胎免疫耐受。Objective To study the role of adoptive transfer of embryo antigen-tolerant T, B cells in pregnant outcome and expression of T_H1 and T_H2 cytokines at materno-fetal interface of the recipient mice. Methods ♀CBA/J×♂DBA/2 matings were recruited as an abortion-prone model. The pregnant CBA/J females mated with DBA/2 male were injected intraperitioneally with rat isotype IgG and rat anti-mouse CD80, CD86 McAb at day 4 of gestation (time of implantation). Purified T, B cells were obtained from spleens of these pregnant CBA/J females at day 9 of gestation, and then injected i. v into the pregnant CBA/J females mated with DBA/2 males at day 4 of gestation. The expression of T_H1 and T_H2 cytokines at maternal-fetal interface of the recipient mice was analyzed, then the embryo resorption rate was counted at day 14 of gestation. Results A decrease in the production of TNF-α and IFN-γ was accompanied by a parallel increase in the production of IL-4 and IL-10 at maternal-fetal interface after adoptive transfer of either embryo antigen-tolerant T cells or T cells from CBA/J×BALB/c matings. In addition, the adoptive transfer of embryo antigen-tolerant T cells increased fetal viability at a level comparable that of T cells from CBA/J×BALB/c matings. Conclusion The adoptive transfer of embryo antigen-tolerant T cells as well as T cells from CBA/J×BALB/c matings may regulate the balance of T_H1/T_H2 cytokine at maternal-fetal interface of abortion-prone model, form the T_H2 bias, and induce the maternal-fetal immuno-tolerance.
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