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怀孕如何影响自身免疫性疾病的进展?

How pregnancy can affect autoimmune diseases progression?

作者信息

Piccinni Marie-Pierre, Lombardelli Letizia, Logiodice Federica, Kullolli Ornela, Parronchi Paola, Romagnani Sergio

机构信息

Center of Excellence for Research, Transfer and High Education DENOTHE of the University of Florence, Florence, Italy ; Department of Experimental and Clinical Medicine, University of Florence, Largo Brambilla 3, 50134 Florence, Italy.

出版信息

Clin Mol Allergy. 2016 Sep 15;14:11. doi: 10.1186/s12948-016-0048-x. eCollection 2016.

Abstract

Autoimmune disorders are characterized by tissue damage, caused by self-reactivity of different effectors mechanisms of the immune system, namely antibodies and T cells. Their occurrence may be associated with genetic and/or environmental predisposition and to some extent, have implications for fertility and obstetrics. The relationship between autoimmunity and reproduction is bidirectional. This review only addresses the impact of pregnancy on autoimmune diseases and not the influence of autoimmunity on pregnancy development. Th17/Th1-type cells are aggressive and pathogenic in many autoimmune disorders and inflammatory diseases. The immunology of pregnancy underlies the role of Th2-type cytokines to maintain the tolerance of the mother towards the fetal semi-allograft. Non-specific factors, including hormonal changes, favor a switch to Th2-type cytokine profile. In pregnancy Th2, Th17/Th2 and Treg cells accumulate in the decidua but may also be present in the mother's circulation and can regulate autoimmune responses influencing the progression of autoimmune diseases.

摘要

自身免疫性疾病的特征是由免疫系统的不同效应机制(即抗体和T细胞)的自身反应性导致组织损伤。它们的发生可能与遗传和/或环境易感性有关,并且在一定程度上对生育和产科有影响。自身免疫与生殖之间的关系是双向的。本综述仅探讨妊娠对自身免疫性疾病的影响,而非自身免疫对妊娠发展的影响。Th17/Th1型细胞在许多自身免疫性疾病和炎症性疾病中具有侵袭性和致病性。妊娠免疫学揭示了Th2型细胞因子在维持母亲对胎儿半同种异体移植物耐受性方面的作用。包括激素变化在内的非特异性因素有利于向Th2型细胞因子谱转变。在妊娠期间,Th2、Th17/Th2和调节性T细胞在蜕膜中积聚,但也可能存在于母亲的循环中,并可调节自身免疫反应,影响自身免疫性疾病的进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d8a/5025626/19214e14af76/12948_2016_48_Fig1_HTML.jpg

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