The dysfunction of CD4(+)CD25(+) regulatory T cells contributes to the abortion of mice caused by Toxoplasma gondii excreted-secreted antigens in early pregnancy.

Toxoplasma gondii is an opportunistic intracellular parasite that is highly prevalent in human and warm-blooded animals throughout the world, leading to potentially severe congenital infections. Although the abortion caused by T. gondii is believed to be dependent on the timing of maternal infection...

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Autores principales:	Jin-ling Chen, Yi-yue Ge, Jie Zhang, Xiao-yan Qiu, Jing-fan Qiu, Jiang-ping Wu, Yong Wang
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2013
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/47648c9eec4245e4a67762b8216c3548
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spelling	oai:doaj.org-article:47648c9eec4245e4a67762b8216c35482021-11-18T07:37:22ZThe dysfunction of CD4(+)CD25(+) regulatory T cells contributes to the abortion of mice caused by Toxoplasma gondii excreted-secreted antigens in early pregnancy.1932-620310.1371/journal.pone.0069012https://doaj.org/article/47648c9eec4245e4a67762b8216c35482013-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23874852/?tool=EBIhttps://doaj.org/toc/1932-6203Toxoplasma gondii is an opportunistic intracellular parasite that is highly prevalent in human and warm-blooded animals throughout the world, leading to potentially severe congenital infections. Although the abortion caused by T. gondii is believed to be dependent on the timing of maternal infection during pregnancy, the mechanism remains unclear. This study was focused on the effects of T. gondii excreted-secreted antigens on pregnant outcomes and CD4(+)CD25(+) Foxp3(+) regulatory T cells at different stages of pregnancy. The results showed that in mice the frequency and suppressive function of CD4(+)CD25(+) regulatory cells were diminished after injection of T. gondii excreted-secreted antigens at early and intermediate stages of pregnancy. The abortion caused by T. gondii excreted-secreted antigens at early pregnancy could be partly prevented by adoptively transferring of CD4(+)CD25(+) cells from the mice injected with T. gondii excreted-secreted antigens at late pregnancy, but not from the mice with the same treatment at early pregnancy. Furthermore, T. gondii excreted-secreted antigens induced apoptosis of CD4(+)CD25(+) regulatory cells of mice in early and intermediate stages of pregnancy by down-regulating their Bcl-2 expressions and Bcl-2/Bax ratio. This study provides new insights into the mechanism that T. gondii infection is the high risk factor for abortion in early pregnancy.Jin-ling ChenYi-yue GeJie ZhangXiao-yan QiuJing-fan QiuJiang-ping WuYong WangPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 8, Iss 7, p e69012 (2013)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Jin-ling Chen Yi-yue Ge Jie Zhang Xiao-yan Qiu Jing-fan Qiu Jiang-ping Wu Yong Wang The dysfunction of CD4(+)CD25(+) regulatory T cells contributes to the abortion of mice caused by Toxoplasma gondii excreted-secreted antigens in early pregnancy.
description	Toxoplasma gondii is an opportunistic intracellular parasite that is highly prevalent in human and warm-blooded animals throughout the world, leading to potentially severe congenital infections. Although the abortion caused by T. gondii is believed to be dependent on the timing of maternal infection during pregnancy, the mechanism remains unclear. This study was focused on the effects of T. gondii excreted-secreted antigens on pregnant outcomes and CD4(+)CD25(+) Foxp3(+) regulatory T cells at different stages of pregnancy. The results showed that in mice the frequency and suppressive function of CD4(+)CD25(+) regulatory cells were diminished after injection of T. gondii excreted-secreted antigens at early and intermediate stages of pregnancy. The abortion caused by T. gondii excreted-secreted antigens at early pregnancy could be partly prevented by adoptively transferring of CD4(+)CD25(+) cells from the mice injected with T. gondii excreted-secreted antigens at late pregnancy, but not from the mice with the same treatment at early pregnancy. Furthermore, T. gondii excreted-secreted antigens induced apoptosis of CD4(+)CD25(+) regulatory cells of mice in early and intermediate stages of pregnancy by down-regulating their Bcl-2 expressions and Bcl-2/Bax ratio. This study provides new insights into the mechanism that T. gondii infection is the high risk factor for abortion in early pregnancy.
format	article
author	Jin-ling Chen Yi-yue Ge Jie Zhang Xiao-yan Qiu Jing-fan Qiu Jiang-ping Wu Yong Wang
author_facet	Jin-ling Chen Yi-yue Ge Jie Zhang Xiao-yan Qiu Jing-fan Qiu Jiang-ping Wu Yong Wang
author_sort	Jin-ling Chen
title	The dysfunction of CD4(+)CD25(+) regulatory T cells contributes to the abortion of mice caused by Toxoplasma gondii excreted-secreted antigens in early pregnancy.
title_short	The dysfunction of CD4(+)CD25(+) regulatory T cells contributes to the abortion of mice caused by Toxoplasma gondii excreted-secreted antigens in early pregnancy.
title_full	The dysfunction of CD4(+)CD25(+) regulatory T cells contributes to the abortion of mice caused by Toxoplasma gondii excreted-secreted antigens in early pregnancy.
title_fullStr	The dysfunction of CD4(+)CD25(+) regulatory T cells contributes to the abortion of mice caused by Toxoplasma gondii excreted-secreted antigens in early pregnancy.
title_full_unstemmed	The dysfunction of CD4(+)CD25(+) regulatory T cells contributes to the abortion of mice caused by Toxoplasma gondii excreted-secreted antigens in early pregnancy.
title_sort	dysfunction of cd4(+)cd25(+) regulatory t cells contributes to the abortion of mice caused by toxoplasma gondii excreted-secreted antigens in early pregnancy.
publisher	Public Library of Science (PLoS)
publishDate	2013
url	https://doaj.org/article/47648c9eec4245e4a67762b8216c3548
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The dysfunction of CD4(+)CD25(+) regulatory T cells contributes to the abortion of mice caused by Toxoplasma gondii excreted-secreted antigens in early pregnancy.

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