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从免疫系统到情绪障碍,特别是由 CD4 T 细胞介导的。

From the immune system to mood disorders especially induced by : CD4 T cell as a bridge.

机构信息

Department of Pathogen Biology, School of Medicine, Nantong University, Nantong, Jiangsu, China.

出版信息

Front Cell Infect Microbiol. 2023 Apr 3;13:1078984. doi: 10.3389/fcimb.2023.1078984. eCollection 2023.

DOI:10.3389/fcimb.2023.1078984
PMID:37077528
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10106765/
Abstract

(), a ubiquitous and obligatory intracellular protozoa, not only alters peripheral immune status, but crosses the blood-brain barrier to trigger brain parenchymal injury and central neuroinflammation to establish latent cerebral infection in humans and other vertebrates. Recent findings underscore the strong correlation between alterations in the peripheral and central immune environment and mood disorders. Th17 and Th1 cells are important pro-inflammatory cells that can drive the pathology of mood disorders by promoting neuroinflammation. As opposed to Th17 and Th1, regulatory T cells have inhibitory inflammatory and neuroprotective functions that can ameliorate mood disorders. induces neuroinflammation, which can be mediated by CD4 T cells (such as Tregs, Th17, Th1, and Th2). Though the pathophysiology and treatment of mood disorder have been currently studied, emerging evidence points to unique role of CD4 T cells in mood disorder, especially those caused by infection. In this review, we explore some recent studies that extend our understanding of the relationship between mood disorders and .

摘要

(),一种普遍存在且必需的细胞内原生动物,不仅改变外周免疫状态,还能穿过血脑屏障引发脑实质损伤和中枢神经炎症,在人类和其他脊椎动物中建立潜伏性脑感染。最近的发现强调了外周和中枢免疫环境改变与情绪障碍之间的强烈相关性。Th17 和 Th1 细胞是重要的促炎细胞,可通过促进神经炎症来驱动情绪障碍的病理。与 Th17 和 Th1 相反,调节性 T 细胞具有抑制炎症和神经保护功能,可以改善情绪障碍。可诱导神经炎症,这可以通过 CD4 T 细胞(如 Tregs、Th17、Th1 和 Th2)介导。尽管情绪障碍的病理生理学和治疗方法目前已经在研究中,但新出现的证据表明 CD4 T 细胞在情绪障碍中具有独特的作用,尤其是由感染引起的情绪障碍。在这篇综述中,我们探讨了一些最近的研究,这些研究扩展了我们对情绪障碍与之间关系的理解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50bc/10106765/6e3086780476/fcimb-13-1078984-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50bc/10106765/ee837f3cc2d7/fcimb-13-1078984-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50bc/10106765/6e3086780476/fcimb-13-1078984-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50bc/10106765/ee837f3cc2d7/fcimb-13-1078984-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50bc/10106765/6e3086780476/fcimb-13-1078984-g002.jpg

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