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2
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Cytotherapy. 2007;9(2):144-57. doi: 10.1080/14653240601145223.
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PIM1 kinase phosphorylates the human transcription factor FOXP3 at serine 422 to negatively regulate its activity under inflammation.PIM1激酶使人类转录因子FOXP3的丝氨酸422位点发生磷酸化，从而在炎症状态下对其活性进行负向调控。
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本文引用的文献

1
Differential impact of mammalian target of rapamycin inhibition on CD4+CD25+Foxp3+ regulatory T cells compared with conventional CD4+ T cells.与传统CD4+ T细胞相比，雷帕霉素哺乳动物靶点抑制对CD4+CD25+Foxp3+调节性T细胞的不同影响。
Blood. 2008 Jan 1;111(1):453-62. doi: 10.1182/blood-2007-06-094482. Epub 2007 Oct 29.
2
Regulatory T-cell immunotherapy for tolerance to self antigens and alloantigens in humans.用于人类对自身抗原和同种异体抗原产生耐受性的调节性T细胞免疫疗法。
Nat Rev Immunol. 2007 Aug;7(8):585-98. doi: 10.1038/nri2138.
3
Foxp3 controls regulatory T-cell function by interacting with AML1/Runx1.Foxp3通过与AML1/Runx1相互作用来控制调节性T细胞的功能。
Nature. 2007 Apr 5;446(7136):685-9. doi: 10.1038/nature05673. Epub 2007 Mar 21.
4
Engineering artificial antigen-presenting cells to express a diverse array of co-stimulatory molecules.工程化人工抗原呈递细胞以表达多种共刺激分子。
Mol Ther. 2007 May;15(5):981-8. doi: 10.1038/mt.sj.6300134. Epub 2007 Mar 20.
5
Genome-wide analysis of Foxp3 target genes in developing and mature regulatory T cells.发育中和成熟调节性T细胞中Foxp3靶基因的全基因组分析。
Nature. 2007 Feb 22;445(7130):936-40. doi: 10.1038/nature05563. Epub 2007 Jan 21.
6
Profiling of CD4+, CD8+, and CD4+CD25+CD45RO+FoxP3+ T cells in patients with malignant glioma reveals differential expression of the immunologic transcriptome compared with T cells from healthy volunteers.恶性胶质瘤患者中CD4 +、CD8 +以及CD4 + CD25 + CD45RO + FoxP3 + T细胞的分析显示，与健康志愿者的T细胞相比，免疫转录组存在差异表达。
Clin Cancer Res. 2006 Dec 15;12(24):7306-15. doi: 10.1158/1078-0432.CCR-06-1727.
7
Selective survival of naturally occurring human CD4+CD25+Foxp3+ regulatory T cells cultured with rapamycin.用雷帕霉素培养的天然存在的人类CD4+CD25+Foxp3+调节性T细胞的选择性存活
J Immunol. 2007 Jan 1;178(1):320-9. doi: 10.4049/jimmunol.178.1.320.
8
Rapamycin promotes expansion of functional CD4+CD25+FOXP3+ regulatory T cells of both healthy subjects and type 1 diabetic patients.雷帕霉素可促进健康受试者和1型糖尿病患者功能性CD4+CD25+FOXP3+调节性T细胞的扩增。
J Immunol. 2006 Dec 15;177(12):8338-47. doi: 10.4049/jimmunol.177.12.8338.
9
FOXP3 controls regulatory T cell function through cooperation with NFAT.FOXP3通过与NFAT协同作用来控制调节性T细胞的功能。
Cell. 2006 Jul 28;126(2):375-87. doi: 10.1016/j.cell.2006.05.042.
10
Rapamycin-mediated enrichment of T cells with regulatory activity in stimulated CD4+ T cell cultures is not due to the selective expansion of naturally occurring regulatory T cells but to the induction of regulatory functions in conventional CD4+ T cells.在受刺激的CD4+ T细胞培养物中，雷帕霉素介导的具有调节活性的T细胞富集并非由于天然存在的调节性T细胞的选择性扩增，而是由于在传统CD4+ T细胞中诱导了调节功能。
J Immunol. 2006 Jul 15;177(2):944-9. doi: 10.4049/jimmunol.177.2.944.

前沿：Foxp3介导的pim 2诱导使人类调节性T细胞在雷帕霉素作用下优先扩增。

Cutting edge: Foxp3-mediated induction of pim 2 allows human T regulatory cells to preferentially expand in rapamycin.

作者信息

Basu Samik, Golovina Tatiana, Mikheeva Tatiana, June Carl H, Riley James L

机构信息

Abramson Family Cancer Research Institute and Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, 421 Curie Boulevard, Philadelphia, PA 19104, USA.

出版信息

J Immunol. 2008 May 1;180(9):5794-8. doi: 10.4049/jimmunol.180.9.5794.

DOI:10.4049/jimmunol.180.9.5794
PMID:18424697
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2504517/
Abstract

Addition of rapamycin to cultures of expanding natural CD4+CD25+Foxp3+ T regulatory cells (Tregs) helps maintain their suppressive activity, but the underlying mechanism is unclear. Pim 2 is a serine/threonine kinase that can confer rapamycin resistance. Unexpectedly, pim 2 was found to be constitutively expressed in freshly isolated, resting Tregs, but not in CD4+CD25- T effector cells. Introduction of Foxp3, but not Foxp3Delta2, into effector T cells induced pim 2 expression and conferred preferential expansion in the presence of rapamycin, indicating that Foxp3 can regulate pim 2 expression. Finally, we determined there is a positive correlation between Treg expansion and Foxp3 expression in the presence of rapamycin. Together, these results indicate that Tregs are programmed to be resistant to rapamycin, providing further rationale for why this immunosuppressive drug should be used in conjunction with expanded Tregs.

摘要

将雷帕霉素添加到正在扩增的天然CD4+CD25+Foxp3+调节性T细胞（Tregs）培养物中有助于维持其抑制活性，但其潜在机制尚不清楚。Pim 2是一种丝氨酸/苏氨酸激酶，可赋予雷帕霉素抗性。出乎意料的是，发现Pim 2在新鲜分离的静息Tregs中组成性表达，但在CD4+CD25-T效应细胞中不表达。将Foxp3而非Foxp3Delta2引入效应T细胞可诱导Pim 2表达，并在存在雷帕霉素的情况下赋予优先扩增能力，表明Foxp3可调节Pim 2表达。最后，我们确定在存在雷帕霉素的情况下，Treg扩增与Foxp3表达之间存在正相关。总之，这些结果表明Tregs被编程为对雷帕霉素具有抗性，这为为何这种免疫抑制药物应与扩增的Tregs联合使用提供了进一步的理论依据。