• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

转化生长因子β1诱导的CD4+CD25+调节性T细胞的过继转移可预防免疫反应介导的自然流产。

Adoptive transfer of transforming growth factor-?1-induced CD4+CD25+ regulatory T cells prevents immune response-mediated spontaneous abortion.

作者信息

Qiu Tian, Teng Yincheng, Wang Yudong, Xu Liang

出版信息

Reprod Fertil Dev. 2015 May 14. doi: 10.1071/RD14503.

DOI:10.1071/RD14503
PMID:25969999
Abstract

The effects of adoptive transfer of transforming growth factor (TGF)-β1-induced regulatory T (Treg) cells in preventing spontaneous abortion in mice were investigated. CD4+CD25- cells were isolated from the spleens of pregnant CBA/J mice and induced into Treg cells positive for CD4, CD25 and forkhead box P3 (FOXP3) ex vivo using interleukin (IL)-2 and TGF-β1. CBA/J mice were mated with DBA/2J mice to establish a model of spontaneous abortion and, on the first day of pregnancy, mice were injected intravenously with 2 × 105 either freshly isolated Treg cells or those induced with TGF-β1. After 14 days, the surviving and reabsorbed fetuses in both groups were counted, and serum cytokine concentrations were measured by ELISA. Adoptive transfer of CD4+CD25+ or TGF-β1-induced Treg cells significantly reduced the fetal resorption rate, increased serum IL-10 and TGF-β1 concentrations and decreased interferon-γ levels. In conclusion, the results of the present study indicate that adoptive transfer of TGF-β1-induced Treg cells prevents spontaneous abortion in mice by increasing the secretion of T helper (Th) 2 cytokines and decreasing the secretion of Th1 cytokines.

摘要

研究了过继转移转化生长因子(TGF)-β1诱导的调节性T(Treg)细胞对预防小鼠自然流产的作用。从怀孕CBA/J小鼠的脾脏中分离出CD4+CD25-细胞,并在体外使用白细胞介素(IL)-2和TGF-β1将其诱导为CD4、CD25和叉头框P3(FOXP3)阳性的Treg细胞。将CBA/J小鼠与DBA/2J小鼠交配以建立自然流产模型,在怀孕的第一天,给小鼠静脉注射2×105个新鲜分离的Treg细胞或用TGF-β1诱导的Treg细胞。14天后,统计两组中存活和吸收的胎儿数量,并通过酶联免疫吸附测定法测量血清细胞因子浓度。过继转移CD4+CD25+或TGF-β1诱导的Treg细胞可显著降低胎儿吸收率,提高血清IL-10和TGF-β1浓度,并降低干扰素-γ水平。总之,本研究结果表明,过继转移TGF-β1诱导的Treg细胞可通过增加辅助性T(Th)2细胞因子的分泌和减少Th1细胞因子的分泌来预防小鼠自然流产。

相似文献

1
Adoptive transfer of transforming growth factor-?1-induced CD4+CD25+ regulatory T cells prevents immune response-mediated spontaneous abortion.转化生长因子β1诱导的CD4+CD25+调节性T细胞的过继转移可预防免疫反应介导的自然流产。
Reprod Fertil Dev. 2015 May 14. doi: 10.1071/RD14503.
2
Adoptive transfer of CD4+CD25+ regulatory T cells for prevention and treatment of spontaneous abortion.采用 CD4+CD25+ 调节性 T 细胞进行主动转移,以预防和治疗自然流产。
Eur J Obstet Gynecol Reprod Biol. 2012 Apr;161(2):177-81. doi: 10.1016/j.ejogrb.2011.12.023. Epub 2012 Jan 18.
3
Effect of adoptive transfer of CD4CD25Foxp3 Treg induced by trichostatin A on the prevention of spontaneous abortion.三氟乙酰螺旋霉素 A 诱导的 CD4CD25Foxp3 Treg 过继转移对预防自然流产的影响。
J Reprod Immunol. 2019 Feb;131:30-35. doi: 10.1016/j.jri.2018.12.002. Epub 2018 Dec 26.
4
Abnormal T-cell reactivity against paternal antigens in spontaneous abortion: adoptive transfer of pregnancy-induced CD4+CD25+ T regulatory cells prevents fetal rejection in a murine abortion model.自然流产中针对父源抗原的异常T细胞反应性:妊娠诱导的CD4+CD25+调节性T细胞的过继转移可预防小鼠流产模型中的胎儿排斥反应。
Am J Pathol. 2005 Mar;166(3):811-22. doi: 10.1016/S0002-9440(10)62302-4.
5
Adoptive transfer of pregnancy-induced CD4+CD25+ regulatory T cells reverses the increase in abortion rate caused by interleukin 17 in the CBA/JxBALB/c mouse model.在CBA/JxBALB/c小鼠模型中,过继转移妊娠诱导的CD4+CD25+调节性T细胞可逆转白细胞介素17所导致的流产率升高。
Hum Reprod. 2014 May;29(5):946-52. doi: 10.1093/humrep/deu014. Epub 2014 Feb 20.
6
Adoptive cell therapy with induced regulatory T cells normalises the abortion rate in abortion-prone mice.诱导调节性 T 细胞的过继细胞疗法可使易流产的小鼠流产率正常化。
Reprod Fertil Dev. 2021 Feb;33(3):220-228. doi: 10.1071/RD20063.
7
Progesterone modulates CD4 CD25 FoxP3 regulatory T Cells and TGF-β1 in the maternal-fetal interface of the late pregnant mouse.孕激素调节晚期妊娠小鼠母胎界面 CD4+CD25+FoxP3+调节性 T 细胞及 TGF-β1 的表达。
Am J Reprod Immunol. 2022 Aug;88(2):e13541. doi: 10.1111/aji.13541. Epub 2022 Apr 5.
8
Granulocytic myeloid-derived suppressor cells maintain feto-maternal tolerance by inducing Foxp3 expression in CD4+CD25-T cells by activation of the TGF-β/β-catenin pathway.粒细胞髓源性抑制细胞通过激活TGF-β/β-连环蛋白途径诱导CD4+CD25-T细胞中Foxp3表达,从而维持母胎耐受。
Mol Hum Reprod. 2016 Jul;22(7):499-511. doi: 10.1093/molehr/gaw026. Epub 2016 Mar 25.
9
Equine CD4(+) CD25(high) T cells exhibit regulatory activity by close contact and cytokine-dependent mechanisms in vitro.马的 CD4(+) CD25(high) T 细胞通过体外的紧密接触和细胞因子依赖的机制表现出调节活性。
Immunology. 2011 Nov;134(3):292-304. doi: 10.1111/j.1365-2567.2011.03489.x.
10
Effect of TGF-β1 on blood CD4CD25 regulatory T cell proliferation and Foxp3 expression during non-small cell lung cancer blood metastasis.转化生长因子-β1对非小细胞肺癌血行转移过程中血液CD4CD25调节性T细胞增殖及叉头框蛋白3表达的影响
Exp Ther Med. 2018 Aug;16(2):1403-1410. doi: 10.3892/etm.2018.6306. Epub 2018 Jun 13.

引用本文的文献

1
IL-27/Blimp-1 axis regulates the differentiation and function of Tim-3+ Tregs during early pregnancy.IL-27/Blimp-1 轴调节妊娠早期 Tim-3+Tregs 的分化和功能。
JCI Insight. 2024 Aug 22;9(16):e179233. doi: 10.1172/jci.insight.179233.
2
Evaluation of Th17 and Treg cytokines in patients with unexplained recurrent pregnancy loss.不明原因复发性流产患者中Th17和调节性T细胞细胞因子的评估
J Clin Transl Res. 2022 May 25;8(3):256-265. eCollection 2022 Jun 29.
3
Role of hormones in the pregnancy and sex-specific outcomes to infections with respiratory viruses.
激素在妊娠和呼吸道病毒感染的性别特异性结局中的作用。
Immunol Rev. 2022 Jul;308(1):123-148. doi: 10.1111/imr.13078. Epub 2022 Apr 4.
4
Regulatory T Cells in Pregnancy: It Is Not All About FoxP3.妊娠中的调节性 T 细胞:并非全关乎 FoxP3。
Front Immunol. 2020 Jun 23;11:1182. doi: 10.3389/fimmu.2020.01182. eCollection 2020.
5
The Effect of TGF-β on Treg Cells in Adverse Pregnancy Outcome upon Infection.转化生长因子-β对感染所致不良妊娠结局中调节性T细胞的影响。
Front Microbiol. 2017 May 26;8:901. doi: 10.3389/fmicb.2017.00901. eCollection 2017.