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本文引用的文献

1
Depletion with PC61 mAb before Toxoplasma gondii infection eliminates mainly Tregs in BALB/c mice, but activated cells in C57BL/6J mice.在弓形虫感染前用PC61单克隆抗体清除细胞,主要清除BALB/c小鼠中的调节性T细胞,但清除C57BL/6J小鼠中的活化细胞。
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CD4+FoxP3+ regulatory T-cells in cerebral ischemic stroke.脑缺血性卒中中的 CD4+FoxP3+调节性 T 细胞。
Metab Brain Dis. 2011 Mar;26(1):87-90. doi: 10.1007/s11011-010-9226-6. Epub 2010 Nov 17.
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Traumatic brain injury--football, warfare, and long-term effects.创伤性脑损伤——足球、战争及长期影响
N Engl J Med. 2010 Sep 30;363(14):1293-6. doi: 10.1056/NEJMp1007051. Epub 2010 Sep 22.
4
TGF-beta-induced myelin peptide-specific regulatory T cells mediate antigen-specific suppression of induction of experimental autoimmune encephalomyelitis.TGF-β 诱导的髓鞘肽特异性调节性 T 细胞介导实验性自身免疫性脑脊髓炎诱导的抗原特异性抑制。
J Immunol. 2010 Jun 15;184(12):6629-36. doi: 10.4049/jimmunol.0904044. Epub 2010 May 7.
5
DAPK1 interaction with NMDA receptor NR2B subunits mediates brain damage in stroke.DAPK1 与 NMDA 受体 NR2B 亚基相互作用介导中风中的脑损伤。
Cell. 2010 Jan 22;140(2):222-34. doi: 10.1016/j.cell.2009.12.055.
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In vivo depletion of CD4+FOXP3+ Treg cells by the PC61 anti-CD25 monoclonal antibody is mediated by FcgammaRIII+ phagocytes.PC61 抗 CD25 单克隆抗体通过 FcγRIII+吞噬细胞在体内耗竭 CD4+FOXP3+Treg 细胞。
Eur J Immunol. 2010 Mar;40(3):780-6. doi: 10.1002/eji.200939613.
7
Antigen presentation in the thymus for positive selection and central tolerance induction.胸腺中的抗原呈递用于阳性选择和中枢耐受诱导。
Nat Rev Immunol. 2009 Dec;9(12):833-44. doi: 10.1038/nri2669.
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Considering the evolution of regeneration in the central nervous system.考虑中枢神经系统再生的演变。
Nat Rev Neurosci. 2009 Oct;10(10):713-23. doi: 10.1038/nrn2707.
9
Enhancement of T-cell-mediated anti-tumour immunity via the ectopically expressed glucocorticoid-induced tumour necrosis factor receptor-related receptor ligand (GITRL) on tumours.通过肿瘤上异位表达的糖皮质激素诱导的肿瘤坏死因子受体相关受体配体(GITRL)增强T细胞介导的抗肿瘤免疫。
Immunology. 2009 Aug;127(4):489-99. doi: 10.1111/j.1365-2567.2008.03036.x.
10
Natural and adaptive foxp3+ regulatory T cells: more of the same or a division of labor?天然和适应性Foxp3+调节性T细胞:是同质性还是分工不同?
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中枢神经系统损伤中的调节性 T 细胞:简单、复杂和混淆。

Regulatory T cells in CNS injury: the simple, the complex and the confused.

机构信息

Neuroscience Graduate Program and Medical Scientist Training Program, Department of Neuroscience, University of Virginia, Charlottesville, VA 22908, USA.

出版信息

Trends Mol Med. 2011 Oct;17(10):541-7. doi: 10.1016/j.molmed.2011.05.012. Epub 2011 Jul 7.

DOI:10.1016/j.molmed.2011.05.012
PMID:21741881
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3189297/
Abstract

Regulatory CD4(+)CD25(+)Foxp3(+) T cells (Tregs) have been the focus of significant attention for their role in controlling immune responses. Although knowledge of Treg biology has burgeoned, wide gaps remain in our understanding of Treg function under both normal and pathological conditions. Pioneering studies demonstrated roles for Tregs in cancer and autoimmune diseases, including experimental autoimmune encephalitis, and this knowledge is often applied to other pathologies including neurodegenerative conditions. However, differences between immunity in neurodegeneration and in malignancy or autoimmunity are often neglected. Thus, Treg manipulations in central nervous system (CNS) neurodegenerative conditions often yield unexpected outcomes. In this piece, we explore how the immunology of neurodegeneration differs from that of cancer and autoimmunity and how these differences create confusion about the role of Tregs in neurodegenerative conditions.

摘要

调节性 CD4(+)CD25(+)Foxp3(+)T 细胞 (Tregs) 因其在控制免疫反应中的作用而受到广泛关注。尽管 Treg 生物学的知识已经迅速发展,但我们对 Treg 在正常和病理条件下的功能仍存在很大的理解差距。开创性的研究表明 Tregs 在癌症和自身免疫性疾病中的作用,包括实验性自身免疫性脑脊髓炎,并且这些知识经常应用于其他病理学,包括神经退行性疾病。然而,神经退行性疾病中的免疫与恶性肿瘤或自身免疫中的免疫之间的差异常常被忽视。因此,中枢神经系统 (CNS) 神经退行性疾病中的 Treg 操作常常产生意想不到的结果。在这篇文章中,我们探讨了神经退行性疾病的免疫学与癌症和自身免疫性疾病的免疫学有何不同,以及这些差异如何导致人们对 Tregs 在神经退行性疾病中的作用产生混淆。