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白细胞介素-6/白细胞介素-12细胞因子超家族和调节性淋巴细胞在中枢神经系统自身免疫性疾病的病因和抑制中起关键作用。

IL-6/IL-12 superfamily of cytokines and regulatory lymphocytes play critical roles in the etiology and suppression of CNS autoimmune diseases.

作者信息

Yadav Manoj Kumar, Singh Samara P, Egwuagu Charles E

机构信息

Molecular Immunology Section, Laboratory of Immunology, National Eye Institute (NEI), National Institutes of Health (NIH), Bethesda, MD, United States.

出版信息

Front Immunol. 2025 Mar 6;16:1514080. doi: 10.3389/fimmu.2025.1514080. eCollection 2025.

DOI:10.3389/fimmu.2025.1514080
PMID:40114923
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11922825/
Abstract

Cytokines influence cell-fate decisions of naïve lymphocytes and determine outcome of immune responses by transducing signals that regulate the initiation, intensity and duration of immune responses. However, aberrant regulation of physiological levels of cytokines contribute to the development of autoimmune and other inflammatory diseases. The Interleukin 6 (IL-6)/IL-12 superfamily of cytokines have a profound influence on all aspects of host immunity and our focus in this review is on the signaling pathways that mediate their functions, with emphasis on how this enigmatic family of cytokines promote or suppress inflammation depending on the physiological context. We also describe regulatory lymphocyte populations that suppress neuroinflammatory diseases by producing cytokines, such as IL-27 (i27-Breg) or IL-35 (i35-Breg and iT35). We conclude with emerging immunotherapies like STAT-specific Nanobodies, Exosomes and Breg therapy that ameliorate CNS autoimmune diseases in preclinical studies.

摘要

细胞因子通过转导调节免疫反应起始、强度和持续时间的信号,影响初始淋巴细胞的细胞命运决定,并决定免疫反应的结果。然而,细胞因子生理水平的异常调节会导致自身免疫性疾病和其他炎症性疾病的发生。白细胞介素6(IL-6)/白细胞介素12细胞因子超家族对宿主免疫的各个方面都有深远影响,在本综述中,我们关注介导其功能的信号通路,重点是这个神秘的细胞因子家族如何根据生理背景促进或抑制炎症。我们还描述了通过产生细胞因子(如IL-27(i27-Breg)或IL-35(i35-Breg和iT35))来抑制神经炎症性疾病的调节性淋巴细胞群体。我们以在临床前研究中改善中枢神经系统自身免疫性疾病的新兴免疫疗法(如STAT特异性纳米抗体、外泌体和调节性B细胞疗法)作为总结。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bb16/11922825/e556a2a2f6cc/fimmu-16-1514080-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bb16/11922825/a9822fc0faab/fimmu-16-1514080-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bb16/11922825/78d6b916c812/fimmu-16-1514080-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bb16/11922825/35aba57117c5/fimmu-16-1514080-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bb16/11922825/e556a2a2f6cc/fimmu-16-1514080-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bb16/11922825/a9822fc0faab/fimmu-16-1514080-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bb16/11922825/78d6b916c812/fimmu-16-1514080-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bb16/11922825/35aba57117c5/fimmu-16-1514080-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bb16/11922825/e556a2a2f6cc/fimmu-16-1514080-g004.jpg

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