Spontaneous recurrent abortion (SRA) has been treated by means of immunization with paternal or third-party white blood cells, yet the immunological basis for SRA and for the role of immunization protocols in pregnancy outcome remains controversial. To elucidate this question, nine women with SRA were immunized with paternal mononuclear cells and studied before and 2 weeks after immunization. Seven women who became pregnant gave birth to live newborns. Secretion of the T helper 1 cytokines IL-2 and interferon-gamma by patients, mononuclear cells decreased, while production of IL-10 increased. The levels of natural killer and lymphokine-activated killer cell-mediated cytotoxicity were markedly decreased. Monocyte functions such as secretion of IL-1 alpha, tumor necrosis factor alpha, IL-6, and cytotoxic activity decreased concurrently with elevations in IL-10 and transforming growth factor beta secretion. Production of IL-12, a pivotal regulatory cytokine, decreased. Furthermore, B7/1 expression on patients' mononuclear cells was downregulated. This resulted in a decrease in monocyte costimulatory activity of purified T cells with soluble anti-CD3, paralleled by a decline in allogeneic proliferative responses. These results suggest that the improved pregnancy success rate in women with SRA following immunization may be partly related to suppression of cell-mediated immunity and monocyte and natural killer cell activity.

译文

自发性复发性流产 (SRA) 已通过父亲或第三方白细胞预防接种进行治疗,但SRA的免疫学基础以及预防接种方案在妊娠结局中的作用仍存在争议。为了阐明这个问题,对9名患有SRA的妇女进行了父本单核细胞免疫,并在免疫前和免疫后2周进行了研究。七名怀孕的妇女生下了活新生儿。T辅助细胞因子IL-2和干扰素-γ 的分泌由患者,单核细胞减少,而IL-10的产生增加。自然杀伤和淋巴因子激活的杀伤细胞介导的细胞毒性水平显着降低。单核细胞功能 (例如IL-1 α,肿瘤坏死因子 α,IL-6和细胞毒性活性的分泌) 随着IL-10和转化生长因子 β 分泌的升高而降低。IL-12 (一种关键的调节细胞因子) 的产生减少。此外,B7/1在患者单核细胞上的表达下调。这导致具有可溶性anti-CD3的纯化T细胞的单核细胞共刺激活性降低,同时同种异体增殖反应下降。这些结果表明预防接种后SRA妇女的妊娠成功率提高可能部分与抑制细胞介导的免疫,单核细胞和自然杀伤细胞活性有关。

+1
+2
100研值 100研值 ¥99课程
检索文献一次
下载文献一次

去下载>

成功解锁2个技能,为你点赞

《SCI写作十大必备语法》
解决你的SCI语法难题!

技能熟练度+1

视频课《玩转文献检索》
让你成为检索达人!

恭喜完成新手挑战

手机微信扫一扫,添加好友领取

免费领《Endnote文献管理工具+教程》

微信扫码, 免费领取

手机登录

获取验证码
登录