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在实验性自身免疫性脑脊髓炎期间,CD24控制中枢神经系统中自身反应性T细胞的扩增和持续存在。

CD24 controls expansion and persistence of autoreactive T cells in the central nervous system during experimental autoimmune encephalomyelitis.

作者信息

Bai Xue-Feng, Li Ou, Zhou Qunmin, Zhang Huiming, Joshi Pramod S, Zheng Xincheng, Liu Yan, Wang Yin, Zheng Pan, Liu Yang

机构信息

Division of Cancer Immunology, Department of Pathology, Ohio State University Medical Center, 129 Hamilton Hall, 1645 Neil Ave., Columbus 43210, USA.

出版信息

J Exp Med. 2004 Aug 16;200(4):447-58. doi: 10.1084/jem.20040131.

DOI:10.1084/jem.20040131
PMID:15314074
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2211938/
Abstract

In the development of experimental autoimmune encephalomyelitis (EAE), a model for multiple sclerosis (MS), autoreactive T cells must be activated and clonally expand in the lymphoid organs, and then migrate into the central nervous system (CNS) where they undergo further activation. It is unclear whether the autoreactive T cells further expand in the CNS and if so, what interactions are required for this process. We have demonstrated previously that expression by the host cells of the heat-stable antigen (CD24), which was recently identified as a genetic modifier for MS, is essential for their susceptibility to EAE. Here we show that CD24 is essential for local clonal expansion and persistence of T cells after their migration into the CNS, and that expression of CD24 on either hematopoietic cells or nonhematopoietic antigen-presenting cells in the recipient is sufficient to confer susceptibility to EAE.

摘要

在实验性自身免疫性脑脊髓炎(EAE,一种多发性硬化症(MS)模型)的发展过程中,自身反应性T细胞必须在淋巴器官中被激活并克隆性扩增,然后迁移到中枢神经系统(CNS),在那里它们会经历进一步激活。目前尚不清楚自身反应性T细胞在CNS中是否会进一步扩增,如果是,该过程需要哪些相互作用。我们之前已经证明,宿主细胞表达的热稳定抗原(CD24,最近被确定为MS的遗传修饰因子)对于它们对EAE的易感性至关重要。在这里我们表明,CD24对于T细胞迁移到CNS后的局部克隆扩增和持续存在至关重要,并且受体中造血细胞或非造血抗原呈递细胞上CD24的表达足以赋予对EAE的易感性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2dbe/2211938/577a091f7470/20040131f9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2dbe/2211938/a05b62b62c11/20040131f1.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2dbe/2211938/10dc6137e124/20040131f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2dbe/2211938/586cb6086293/20040131f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2dbe/2211938/0850faea7923/20040131f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2dbe/2211938/35bad6fe78d5/20040131f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2dbe/2211938/577a091f7470/20040131f9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2dbe/2211938/a05b62b62c11/20040131f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2dbe/2211938/d1443481aa01/20040131f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2dbe/2211938/11ecd727b85b/20040131f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2dbe/2211938/1364a0e0455e/20040131f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2dbe/2211938/10dc6137e124/20040131f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2dbe/2211938/586cb6086293/20040131f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2dbe/2211938/0850faea7923/20040131f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2dbe/2211938/35bad6fe78d5/20040131f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2dbe/2211938/577a091f7470/20040131f9.jpg

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