Regulatory T cells and the immune pathogenesis of prenatal infection.
Regulatory T cells and the immune pathogenesis of prenatal infection.
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DOI：
10.1530/rep-13-0262
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发表时间：
2013-12
期刊：
影响因子：
--
通讯作者：
Way SS
中科院分区：
文献类型：
--
作者：
Rowe JH;Ertelt JM;Xin L;Way SS
胎盘哺乳动物的怀孕为发育中的胎儿提供了宫内保护、营养和消除代谢废物的特殊综合益处。然而，这些优点还需要持久的策略来减轻表达外源父源抗原的胎儿组织的母体排斥。自从60年前Peter Medawar爵士提出母体免疫耐受性扩大的最初假设以来，已经显示出在母体胎盘界面局部和全身作用的分子和细胞修饰的惊人复杂分类可以沉默潜在有害的母体免疫反应。反过来，在怀孕期间同时保持宿主对无限的潜在病原体的防御也同样重要。幸运的是，对大多数感染的抵抗力在整个妊娠期都得到了无缝的保护。另一方面，最近对具有产前感染独特倾向的病原体的研究揭示了与生殖过程相关的宿主防御中的独特漏洞。使用这些感染来探测妊娠期间的反应，越来越多的研究表明，母体CD4 T细胞的免疫抑制调节亚群决定了产前感染易感性和随后妊娠并发症发病机制之间的相互作用。在此，最近的文献表明，孕妇的必要性调节性T细胞在妊娠诱导的免疫变化，维持胎儿的耐受性进行审查。额外的讨论集中在如何扩展的母体调节性T细胞抑制可能成为利用病原体引起产前感染，感染诱导的免疫激活，可能会减轻胎儿的耐受性和无意中注入敌意到子宫内的保护环境的危险潜力。
Pregnancy in placental mammals offers exceptional comprehensive benefits of in utero protection, nutrition, and elimination of metabolic waste for the developing fetus. However, these advantages also require durable strategies to mitigate maternal rejection of fetal tissue expressing foreign paternal antigens. Since the initial postulate of expanded maternal immune tolerance by Sir Peter Medawar 60 years ago, an amazingly elaborate assortment of molecular and cellular modifications acting both locally at the maternal placental interface and systemically have been shown to silence potentially detrimental maternal immune responses. In turn, simultaneously maintaining host defense against the infinite array of potential pathogens during pregnancy is equally important. Fortunately, resistance against most infections is preserved seamlessly throughout gestation. On the other hand, recent studies on pathogens with unique predisposition for prenatal infection have uncovered distinctive holes in host defense associated with the reproductive process. Using these infections to probe the response during pregnancy, the immune suppressive regulatory subset of maternal CD4 T cells has been increasingly shown to dictate the inter-workings between prenatal infection susceptibility and pathogenesis of ensuing pregnancy complications. Herein, the recent literature suggesting a necessity for maternal regulatory T cells in pregnancy induced immunological shifts that sustain fetal tolerance is reviewed. Additional discussion is focused on how expansion of maternal regulatory T cell suppression may become exploited by pathogens that cause prenatal infection, and the perilous potential of infection induced immune activation that may mitigate fetal tolerance and inadvertently inject hostility into the protective in utero environment.