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CD4(+)CD25(+)Foxp3(+) regulatory T cells regulate immune balance in unexplained recurrent spontaneous abortion via the Toll-like receptor 4/nuclear factor-κB pathway

OBJECTIVE: The present study aimed to evaluate the effects of cluster of differentiation (CD)4(+)CD25(+) forkhead box p3 (Foxp3)(+) regulatory T cells (Tregs) on unexplained recurrent spontaneous abortion (URSA) and the associated mechanisms. METHODS: The proportion of CD4(+)CD25(+)Foxp3(+) Tregs an...

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Autores principales: Qin, Shuang, Li, Li, Liu, Jia, Zhang, Jinrui, Xiao, Qing, Fan, Yujuan, Wei, Xiangcai
Formato: Online Artículo Texto
Lenguaje:English
Publicado: SAGE Publications 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7768580/
https://www.ncbi.nlm.nih.gov/pubmed/33356705
http://dx.doi.org/10.1177/0300060520980940
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author Qin, Shuang
Li, Li
Liu, Jia
Zhang, Jinrui
Xiao, Qing
Fan, Yujuan
Wei, Xiangcai
author_facet Qin, Shuang
Li, Li
Liu, Jia
Zhang, Jinrui
Xiao, Qing
Fan, Yujuan
Wei, Xiangcai
author_sort Qin, Shuang
collection PubMed
description OBJECTIVE: The present study aimed to evaluate the effects of cluster of differentiation (CD)4(+)CD25(+) forkhead box p3 (Foxp3)(+) regulatory T cells (Tregs) on unexplained recurrent spontaneous abortion (URSA) and the associated mechanisms. METHODS: The proportion of CD4(+)CD25(+)Foxp3(+) Tregs and inflammatory cytokine concentrations in the peripheral blood of women with URSA were measured by flow cytometry and enzyme-linked immunosorbent assay, respectively. CBA/JxDBA/2J mating was used to establish an abortion-prone mouse model and the model mice were treated with the Toll-like receptor 4 (TLR4) antagonist E5564 and the TLR4 agonist lipopolysaccharide. RESULTS: The proportion of CD4(+)CD25(+)Foxp3(+) Tregs was decreased and the inflammatory response was increased in women with URSA. In the abortion-prone mouse model, E5564 significantly increased the proportion of CD4(+)CD25(+)Foxp3(+) Tregs, decreased the inflammatory response, and increased Foxp3 mRNA and protein expression. Lipopolysaccharide had adverse effects on the abortion-prone model. CONCLUSIONS: These data suggest that CD4(+)CD25(+)Foxp3(+) Tregs regulate immune homeostasis in URSA via the TLR4/nuclear factor-κB pathway, and that the TLR4 antagonist E5564 may be a novel and potential drug for treating URSA.
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spelling pubmed-77685802021-01-21 CD4(+)CD25(+)Foxp3(+) regulatory T cells regulate immune balance in unexplained recurrent spontaneous abortion via the Toll-like receptor 4/nuclear factor-κB pathway Qin, Shuang Li, Li Liu, Jia Zhang, Jinrui Xiao, Qing Fan, Yujuan Wei, Xiangcai J Int Med Res Prospective Clinical Research Report OBJECTIVE: The present study aimed to evaluate the effects of cluster of differentiation (CD)4(+)CD25(+) forkhead box p3 (Foxp3)(+) regulatory T cells (Tregs) on unexplained recurrent spontaneous abortion (URSA) and the associated mechanisms. METHODS: The proportion of CD4(+)CD25(+)Foxp3(+) Tregs and inflammatory cytokine concentrations in the peripheral blood of women with URSA were measured by flow cytometry and enzyme-linked immunosorbent assay, respectively. CBA/JxDBA/2J mating was used to establish an abortion-prone mouse model and the model mice were treated with the Toll-like receptor 4 (TLR4) antagonist E5564 and the TLR4 agonist lipopolysaccharide. RESULTS: The proportion of CD4(+)CD25(+)Foxp3(+) Tregs was decreased and the inflammatory response was increased in women with URSA. In the abortion-prone mouse model, E5564 significantly increased the proportion of CD4(+)CD25(+)Foxp3(+) Tregs, decreased the inflammatory response, and increased Foxp3 mRNA and protein expression. Lipopolysaccharide had adverse effects on the abortion-prone model. CONCLUSIONS: These data suggest that CD4(+)CD25(+)Foxp3(+) Tregs regulate immune homeostasis in URSA via the TLR4/nuclear factor-κB pathway, and that the TLR4 antagonist E5564 may be a novel and potential drug for treating URSA. SAGE Publications 2020-12-23 /pmc/articles/PMC7768580/ /pubmed/33356705 http://dx.doi.org/10.1177/0300060520980940 Text en © The Author(s) 2020 https://creativecommons.org/licenses/by-nc/4.0/ Creative Commons Non Commercial CC BY-NC: This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage).
spellingShingle Prospective Clinical Research Report
Qin, Shuang
Li, Li
Liu, Jia
Zhang, Jinrui
Xiao, Qing
Fan, Yujuan
Wei, Xiangcai
CD4(+)CD25(+)Foxp3(+) regulatory T cells regulate immune balance in unexplained recurrent spontaneous abortion via the Toll-like receptor 4/nuclear factor-κB pathway
title CD4(+)CD25(+)Foxp3(+) regulatory T cells regulate immune balance in unexplained recurrent spontaneous abortion via the Toll-like receptor 4/nuclear factor-κB pathway
title_full CD4(+)CD25(+)Foxp3(+) regulatory T cells regulate immune balance in unexplained recurrent spontaneous abortion via the Toll-like receptor 4/nuclear factor-κB pathway
title_fullStr CD4(+)CD25(+)Foxp3(+) regulatory T cells regulate immune balance in unexplained recurrent spontaneous abortion via the Toll-like receptor 4/nuclear factor-κB pathway
title_full_unstemmed CD4(+)CD25(+)Foxp3(+) regulatory T cells regulate immune balance in unexplained recurrent spontaneous abortion via the Toll-like receptor 4/nuclear factor-κB pathway
title_short CD4(+)CD25(+)Foxp3(+) regulatory T cells regulate immune balance in unexplained recurrent spontaneous abortion via the Toll-like receptor 4/nuclear factor-κB pathway
title_sort cd4(+)cd25(+)foxp3(+) regulatory t cells regulate immune balance in unexplained recurrent spontaneous abortion via the toll-like receptor 4/nuclear factor-κb pathway
topic Prospective Clinical Research Report
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7768580/
https://www.ncbi.nlm.nih.gov/pubmed/33356705
http://dx.doi.org/10.1177/0300060520980940
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