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Memory cells specific for myelin oligodendrocyte glycoprotein (MOG) govern the transfer of experimental autoimmune encephalomyelitis.针对髓鞘少突胶质细胞糖蛋白（MOG）的记忆细胞可控制实验性自身免疫性脑脊髓炎的转移。
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2
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本文引用的文献

1
Th1, Th17, and Th9 effector cells induce experimental autoimmune encephalomyelitis with different pathological phenotypes.Th1、Th17和Th9效应细胞可诱导出具有不同病理表型的实验性自身免疫性脑脊髓炎。
J Immunol. 2009 Dec 1;183(11):7169-77. doi: 10.4049/jimmunol.0901906. Epub 2009 Nov 4.
2
T-bet is essential for encephalitogenicity of both Th1 and Th17 cells.T-bet对于Th1和Th17细胞的致脑炎能力至关重要。
J Exp Med. 2009 Jul 6;206(7):1549-64. doi: 10.1084/jem.20082584. Epub 2009 Jun 22.
3
IL-17A and IL-17F do not contribute vitally to autoimmune neuro-inflammation in mice.白细胞介素-17A和白细胞介素-17F对小鼠自身免疫性神经炎症并非至关重要。
J Clin Invest. 2009 Jan;119(1):61-9. doi: 10.1172/JCI35997. Epub 2008 Dec 15.
4
Differential regulation of central nervous system autoimmunity by T(H)1 and T(H)17 cells.辅助性T细胞1（Th1）和辅助性T细胞17（Th17）对中枢神经系统自身免疫的差异调节
Nat Med. 2008 Mar;14(3):337-42. doi: 10.1038/nm1715. Epub 2008 Feb 17.
5
Human TH17 lymphocytes promote blood-brain barrier disruption and central nervous system inflammation.人类辅助性T细胞17淋巴细胞会促进血脑屏障破坏和中枢神经系统炎症。
Nat Med. 2007 Oct;13(10):1173-5. doi: 10.1038/nm1651. Epub 2007 Sep 9.
6
T cell-produced transforming growth factor-beta1 controls T cell tolerance and regulates Th1- and Th17-cell differentiation.T细胞产生的转化生长因子-β1控制T细胞耐受性并调节Th1细胞和Th17细胞的分化。
Immunity. 2007 May;26(5):579-91. doi: 10.1016/j.immuni.2007.03.014. Epub 2007 May 3.
7
Reciprocal developmental pathways for the generation of pathogenic effector TH17 and regulatory T cells.致病性效应T辅助细胞17（TH17）和调节性T细胞产生的相互发育途径。
Nature. 2006 May 11;441(7090):235-8. doi: 10.1038/nature04753. Epub 2006 Apr 30.
8
Proliferation and death of oligodendrocytes and myelin proteins are differentially regulated in male and female rodents.少突胶质细胞和髓鞘蛋白的增殖与死亡在雄性和雌性啮齿动物中受到不同的调节。
J Neurosci. 2006 Feb 1;26(5):1439-47. doi: 10.1523/JNEUROSCI.2219-05.2006.
9
Enhanced FoxP3 expression and Treg cell function in pregnant and estrogen-treated mice.怀孕小鼠和接受雌激素处理的小鼠中FoxP3表达增强及调节性T细胞功能增强。
J Neuroimmunol. 2005 Dec 30;170(1-2):85-92. doi: 10.1016/j.jneuroim.2005.08.023. Epub 2005 Oct 25.
10
IL-23 drives a pathogenic T cell population that induces autoimmune inflammation.白细胞介素-23驱动致病性T细胞群体，引发自身免疫性炎症。
J Exp Med. 2005 Jan 17;201(2):233-40. doi: 10.1084/jem.20041257.

针对髓鞘少突胶质细胞糖蛋白（MOG）的记忆细胞可控制实验性自身免疫性脑脊髓炎的转移。

Memory cells specific for myelin oligodendrocyte glycoprotein (MOG) govern the transfer of experimental autoimmune encephalomyelitis.

机构信息

The Ohio State University, Department of Molecular Virology, Immunology, and Medical Genetics, 760 Biomedical Research Tower, 460 W 12th Avenue, Columbus, OH 43210, USA.

出版信息

J Neuroimmunol. 2011 May;234(1-2):84-92. doi: 10.1016/j.jneuroim.2011.02.008. Epub 2011 Apr 3.

DOI:10.1016/j.jneuroim.2011.02.008
PMID:21463904
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3690522/
Abstract

Multiple sclerosis (MS) is an inflammatory disease of the CNS mediated by CD4(+) T cells directed against myelin antigens. Experimental autoimmune encephalomyelitis (EAE) is induced by immunization with myelin antigens like myelin oligodendrocyte glycoprotein (MOG). We have explored the transfer of EAE using MOG(35-55)-specific TCR transgenic (2D2) T cells. Unsorted 2D2 Th1 cells reliably transferred EAE. Further, we found that CD44(hi)CD62L(lo) effector/memory CD4(+) T cells are likely responsible for the disease transfer due to the up-regulation of CD44. Given the importance of MOG in MS pathogenesis, mechanistic insights into adoptively transferred EAE by MOG-specific Th1 cells could prove valuable in MS research.

摘要

多发性硬化症（MS）是一种由中枢神经系统炎症引起的疾病，其介导物是针对髓鞘抗原的 CD4(+)T 细胞。实验性自身免疫性脑脊髓炎（EAE）是通过用髓鞘抗原如髓鞘少突胶质细胞糖蛋白（MOG）免疫诱导产生的。我们使用髓鞘寡糖蛋白（MOG）（35-55）特异性 TCR 转基因（2D2）T 细胞探索了 EAE 的转移。未分选的 2D2Th1 细胞可靠地转移了 EAE。此外，我们发现由于 CD44 的上调，CD44(hi)CD62L(lo)效应/记忆 CD4(+)T 细胞可能是导致疾病转移的原因。鉴于 MOG 在 MS 发病机制中的重要性，通过 MOG 特异性 Th1 细胞进行的过继转移 EAE 的机制见解可能对 MS 研究具有重要价值。