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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

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: Chen, Jin-ling, Ge, Yi-yue, Zhang, Jie, Qiu, Xiao-yan, Qiu, Jing-fan, Wu, Jiang-ping, Wang, Yong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3714236/
https://www.ncbi.nlm.nih.gov/pubmed/23874852
http://dx.doi.org/10.1371/journal.pone.0069012
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author Chen, Jin-ling
Ge, Yi-yue
Zhang, Jie
Qiu, Xiao-yan
Qiu, Jing-fan
Wu, Jiang-ping
Wang, Yong
author_facet Chen, Jin-ling
Ge, Yi-yue
Zhang, Jie
Qiu, Xiao-yan
Qiu, Jing-fan
Wu, Jiang-ping
Wang, Yong
author_sort Chen, Jin-ling
collection PubMed
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.
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spelling pubmed-37142362013-07-19 The Dysfunction of CD4(+)CD25(+) Regulatory T Cells Contributes to the Abortion of Mice Caused by Toxoplasma gondii Excreted-Secreted Antigens in Early Pregnancy Chen, Jin-ling Ge, Yi-yue Zhang, Jie Qiu, Xiao-yan Qiu, Jing-fan Wu, Jiang-ping Wang, Yong PLoS One Research Article 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. Public Library of Science 2013-07-17 /pmc/articles/PMC3714236/ /pubmed/23874852 http://dx.doi.org/10.1371/journal.pone.0069012 Text en © 2013 Chen et al http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.
spellingShingle Research Article
Chen, Jin-ling
Ge, Yi-yue
Zhang, Jie
Qiu, Xiao-yan
Qiu, Jing-fan
Wu, Jiang-ping
Wang, Yong
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 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_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_sort dysfunction of cd4(+)cd25(+) regulatory t cells contributes to the abortion of mice caused by toxoplasma gondii excreted-secreted antigens in early pregnancy
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3714236/
https://www.ncbi.nlm.nih.gov/pubmed/23874852
http://dx.doi.org/10.1371/journal.pone.0069012
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