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本文引用的文献

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Inhibition of cytolytic T lymphocyte proliferation by autologous CD4+/CD25+ regulatory T cells in a colorectal carcinoma patient is mediated by transforming growth factor-beta.在一名结直肠癌患者中，自体CD4⁺/CD25⁺调节性T细胞对细胞溶解性T淋巴细胞增殖的抑制作用是由转化生长因子-β介导的。
Cancer Res. 2002 Sep 15;62(18):5267-72.
2
CD4 regulatory T cells prevent lethal autoimmunity in IL-2Rbeta-deficient mice. Implications for the nonredundant function of IL-2.CD4调节性T细胞可预防IL-2Rβ缺陷小鼠的致死性自身免疫。这对IL-2的非冗余功能具有重要意义。
Immunity. 2002 Aug;17(2):167-78. doi: 10.1016/s1074-7613(02)00367-9.
3
Bacteria-triggered CD4(+) T regulatory cells suppress Helicobacter hepaticus-induced colitis.细菌触发的CD4(+)调节性T细胞抑制肝螺杆菌诱导的结肠炎。
J Exp Med. 2002 Aug 19;196(4):505-15. doi: 10.1084/jem.20020556.
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Donor-type CD4(+)CD25(+) regulatory T cells suppress lethal acute graft-versus-host disease after allogeneic bone marrow transplantation.供体型CD4(+)CD25(+)调节性T细胞可抑制异基因骨髓移植后的致死性急性移植物抗宿主病。
J Exp Med. 2002 Aug 5;196(3):389-99. doi: 10.1084/jem.20020399.
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Phenotype, localization, and mechanism of suppression of CD4(+)CD25(+) human thymocytes.CD4(+)CD25(+) 人胸腺细胞的表型、定位及抑制机制
J Exp Med. 2002 Aug 5;196(3):379-87. doi: 10.1084/jem.20020110.
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Antigen-specific regulatory T cells develop via the ICOS-ICOS-ligand pathway and inhibit allergen-induced airway hyperreactivity.抗原特异性调节性T细胞通过ICOS-ICOS配体途径发育，并抑制变应原诱导的气道高反应性。
Nat Med. 2002 Sep;8(9):1024-32. doi: 10.1038/nm745. Epub 2002 Jul 29.
7
Infectious tolerance: human CD25(+) regulatory T cells convey suppressor activity to conventional CD4(+) T helper cells.感染性耐受：人类CD25(+)调节性T细胞将抑制活性传递给传统CD4(+)辅助性T细胞。
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CD4(+)CD25(+) regulatory T cells can mediate suppressor function in the absence of transforming growth factor beta1 production and responsiveness.CD4(+)CD25(+)调节性T细胞可在不产生及不响应转化生长因子β1的情况下介导抑制功能。
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Depletion of CD4+ CD25+ regulatory cells augments the generation of specific immune T cells in tumor-draining lymph nodes.CD4+ CD25+调节性细胞的耗竭增强了肿瘤引流淋巴结中特异性免疫T细胞的生成。
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CD4(+)CD25(+) immunoregulatory T cells: gene expression analysis reveals a functional role for the glucocorticoid-induced TNF receptor.CD4(+)CD25(+)免疫调节性T细胞：基因表达分析揭示糖皮质激素诱导的肿瘤坏死因子受体的功能作用
Immunity. 2002 Feb;16(2):311-23. doi: 10.1016/s1074-7613(02)00280-7.

在1型糖尿病中，CD4+CD25+调节性T细胞通过转化生长因子-β-转化生长因子-β受体相互作用来控制抗胰岛CD8+T细胞。

CD4+CD25+ T regulatory cells control anti-islet CD8+ T cells through TGF-beta-TGF-beta receptor interactions in type 1 diabetes.

作者信息

Green E Allison, Gorelik Leonid, McGregor Catrin M, Tran Elise H, Flavell Richard A

机构信息

Juvenile Diabetes Research Foundation/Wellcome Trust Diabetes and Inflammation Laboratory, Cambridge Institute for Medical Research, Cambridge University, United Kingdom.

出版信息

Proc Natl Acad Sci U S A. 2003 Sep 16;100(19):10878-83. doi: 10.1073/pnas.1834400100. Epub 2003 Aug 29.

DOI:10.1073/pnas.1834400100
PMID:12949259
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC196896/
Abstract

Pancreatic lymph node-derived CD4+CD25+ T regulatory (Treg) cells inhibit in situ differentiation of islet-reactive CD8+ T cells into cytotoxic T lymphocytes, thereby preventing diabetes progression. The mechanism by which these Treg cells suppress anti-islet CD8+ T cells is unknown. Here, we show by using a CD8+ T cell-mediated model of type 1 diabetes that transforming growth factor (TGF)-beta-TGF-beta receptor signals are critical for CD4+CD25+ Treg cell regulation of autoreactive islet-specific cytotoxic T lymphocytes. Transgenic expression of tumor necrosis factor alpha from birth to 25 days of age in the islets of B6 mice that constitutively express CD80 on their beta cells results in accumulation of CD4+CD25+TGF-beta+ cells exclusively in the islets and pancreatic lymph nodes, which delays diabetes progression. In contrast, expression of tumor necrosis factor alpha until 28 days of age prevents islet accumulation of CD4+CD25+TGF-beta+ Treg cells, resulting in acceleration to diabetes. Furthermore, adoptive transfer experiments demonstrated that CD4+CD25+ Treg cells could not control naïve or activated islet-reactive CD8+ T cells bearing a dominant negative TGF-beta receptor type II. Our data demonstrate that, in vivo, TGF-beta signaling in CD8+ T cells is critical for CD4+CD25+ Treg cell suppression of islet-reactive CD8+ T cells in type 1 diabetes.

摘要

胰腺淋巴结来源的CD4+CD25+调节性T（Treg）细胞可抑制胰岛反应性CD8+T细胞原位分化为细胞毒性T淋巴细胞，从而阻止糖尿病进展。这些Treg细胞抑制抗胰岛CD8+T细胞的机制尚不清楚。在此，我们通过使用1型糖尿病的CD8+T细胞介导模型表明，转化生长因子（TGF）-β-TGF-β受体信号对于CD4+CD25+Treg细胞调节自身反应性胰岛特异性细胞毒性T淋巴细胞至关重要。在β细胞上组成性表达CD80的B6小鼠胰岛中，从出生到25日龄转基因表达肿瘤坏死因子α，导致CD4+CD25+TGF-β+细胞仅在胰岛和胰腺淋巴结中积聚，从而延缓糖尿病进展。相反，直到28日龄表达肿瘤坏死因子α可阻止CD4+CD25+TGF-β+Treg细胞在胰岛中积聚，导致糖尿病加速发展。此外，过继转移实验表明，CD4+CD25+Treg细胞无法控制携带显性负性II型TGF-β受体的幼稚或活化的胰岛反应性CD8+T细胞。我们的数据表明，在体内，CD8+T细胞中的TGF-β信号对于1型糖尿病中CD4+CD25+Treg细胞抑制胰岛反应性CD8+T细胞至关重要。