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白细胞介素-1β在实验性自身免疫性脑脊髓炎和多发性硬化症中作用的新见解

New Insights into the Role of IL-1β in Experimental Autoimmune Encephalomyelitis and Multiple Sclerosis.

作者信息

Lin Chih-Chung, Edelson Brian T

机构信息

Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110.

Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110

出版信息

J Immunol. 2017 Jun 15;198(12):4553-4560. doi: 10.4049/jimmunol.1700263.

DOI:10.4049/jimmunol.1700263
PMID:28583987
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5509030/
Abstract

Multiple sclerosis (MS), and its animal model experimental autoimmune encephalomyelitis, are neuroinflammatory diseases driven by autoreactive pathogenic T cells that elicit demyelination and axonal damage. How T cells acquire pathogenicity and communicate with myeloid cells and cells of the CNS remain unclear. IL-1β is recognized to play an important role in experimental autoimmune encephalomyelitis (EAE) and perhaps MS. Clinical EAE is significantly attenuated in IL-1R-deficient and IL-1β-deficient mice, and IL-1β is found in the blood, cerebrospinal fluid, and CNS lesions of MS patients. In this article, we focus on new reports that elucidate the cellular sources of IL-1β and its actions during EAE, in both lymphoid tissues and within the CNS. Several immune cell types serve as critical producers of IL-1β during EAE, with this cytokine inducing response in both hematopoietic and nonhematopoietic cells. These findings from the EAE model should inspire efforts toward investigating the therapeutic potential of IL-1 blockade in MS.

摘要

多发性硬化症(MS)及其动物模型实验性自身免疫性脑脊髓炎(EAE)是由自身反应性致病T细胞驱动的神经炎症性疾病,这些T细胞会引发脱髓鞘和轴突损伤。T细胞如何获得致病性以及如何与髓样细胞和中枢神经系统细胞进行通信仍不清楚。白细胞介素-1β(IL-1β)被认为在实验性自身免疫性脑脊髓炎(EAE)以及可能在MS中发挥重要作用。在白细胞介素-1受体(IL-1R)缺陷型和IL-1β缺陷型小鼠中,临床EAE明显减轻,并且在MS患者的血液、脑脊液和中枢神经系统病变中发现了IL-1β。在本文中,我们关注一些新报告,这些报告阐明了EAE期间IL-1β在淋巴组织和中枢神经系统内的细胞来源及其作用。在EAE期间,几种免疫细胞类型是IL-1β的关键产生者,这种细胞因子可诱导造血细胞和非造血细胞产生反应。来自EAE模型的这些发现应该会激发人们努力研究IL-1阻断在MS中的治疗潜力。

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