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血红素加氧酶-1 阻断可消除调节性 T 细胞对妊娠的保护作用,并促进树突状细胞的成熟。

Blockage of heme oxygenase-1 abrogates the protective effect of regulatory T cells on murine pregnancy and promotes the maturation of dendritic cells.

机构信息

Department of Experimental Obstetrics and Gynaecology, Medical Faculty, Otto-von Guericke University of Magdeburg, Magdeburg, Germany.

出版信息

PLoS One. 2012;7(8):e42301. doi: 10.1371/journal.pone.0042301. Epub 2012 Aug 10.

DOI:10.1371/journal.pone.0042301
PMID:22900010
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3416808/
Abstract

Regulatory T cells (Treg) play an important role in fetal protection. They expand during normal pregnancy and protect fetal antigens from maternal effector cells. Their effect is associated with the up-regulation of tolerance-associated molecules at the fetal-maternal interface. Among these, Heme Oxygenase-1 (HO-1, coded by Hmox1) is of special importance as its blockage correlates with increased abortion rates and its up-regulation positively affects pregnancy outcome. Here, we aimed to investigate whether the protective effect of Treg is mediated by HO-1 in a mouse model. HO-1 blockage by Zinc Protoporhyrin (ZnPPIX) abrogated the protective effect of Treg transfer. We found that HO-1 is important in maintaining maternal dendritic cells (DCs) in an immature state, which contributes to the expansion of the peripheral Treg population. This brings to light one essential pathway through which Treg mediates the semi-allogeneic fetus tolerance.

摘要

调节性 T 细胞(Treg)在胎儿保护中发挥重要作用。它们在正常妊娠期间扩增,使胎儿抗原免受母体效应细胞的攻击。它们的作用与胎儿-母体界面上与耐受相关的分子的上调有关。在这些分子中,血红素加氧酶-1(HO-1,由 Hmox1 编码)尤为重要,因为其阻断与流产率增加相关,其上调对妊娠结局有积极影响。在这里,我们旨在研究 Treg 的保护作用是否通过 HO-1 在小鼠模型中介导。锌原卟啉(ZnPPIX)阻断 HO-1 可消除 Treg 转移的保护作用。我们发现 HO-1 对于维持母体树突状细胞(DC)处于未成熟状态很重要,这有助于外周 Treg 群体的扩增。这揭示了 Treg 介导半同种异体胎儿耐受的一个重要途径。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/607c/3416808/8c68fcf53419/pone.0042301.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/607c/3416808/2cd77e858e55/pone.0042301.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/607c/3416808/56f8a2fd514c/pone.0042301.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/607c/3416808/3b3c56f71c5c/pone.0042301.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/607c/3416808/b2839a407677/pone.0042301.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/607c/3416808/0c7201e9dc87/pone.0042301.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/607c/3416808/fc26d146941a/pone.0042301.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/607c/3416808/8c68fcf53419/pone.0042301.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/607c/3416808/2cd77e858e55/pone.0042301.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/607c/3416808/56f8a2fd514c/pone.0042301.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/607c/3416808/3b3c56f71c5c/pone.0042301.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/607c/3416808/b2839a407677/pone.0042301.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/607c/3416808/0c7201e9dc87/pone.0042301.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/607c/3416808/fc26d146941a/pone.0042301.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/607c/3416808/8c68fcf53419/pone.0042301.g007.jpg

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