小柯机器人

美国康奈尔大学威尔康奈尔医学Gregory F. Sonnenberg研究组发现抗原呈递性先天淋巴细胞可协调神经炎症。2021年12月1日出版的《自然》杂志发表了该成果。

他们定义了一组炎症组 3 先天淋巴细胞 (ILC3)，它们在多发性硬化症小鼠模型中浸润中枢神经系统。这些 ILC3 来自循环，位于中枢神经系统 (CNS)中浸润的 T 细胞附近，用作重新刺激髓鞘特异性 T 细胞的抗原呈递细胞，并且在患有多发性硬化症的个体中增加。值得注意的是，炎症性 ILC3 的抗原呈递是促进 CNS 中的 T 细胞反应和小鼠模型中多发性硬化样疾病的发展所必需的。

相比之下，外周的常规和组织驻留 ILC3 似乎不会导致疾病诱导，而是限制自身免疫性 T 细胞反应，并在实验性靶向呈递髓鞘抗原时预防多发性硬化症样疾病。总的来说，他们的数据定义了一组炎症性 ILC3，这对于直接促进 CNS 中 T 细胞依赖性神经炎症至关重要，并揭示了利用外周组织驻留 ILC3 预防自身免疫性疾病的潜力。

研究人员表示，CNS中的促炎性 T 细胞与多种脱髓鞘和神经退行性疾病有因果关系，但控制这些反应的途径仍不清楚。

附：英文原文

Title: Antigen-presenting innate lymphoid cells orchestrate neuroinflammation

Author: Grigg, John B., Shanmugavadivu, Arthi, Regen, Tommy, Parkhurst, Christopher N., Ahmed, Anees, Joseph, Ann M., Mazzucco, Michael, Gronke, Konrad, Diefenbach, Andreas, Eberl, Gerard, Vartanian, Timothy, Waisman, Ari, Sonnenberg, Gregory F.

Issue&Volume: 2021-12-01

Abstract: Pro-inflammatory T cells in the central nervous system (CNS) are causally associated with multiple demyelinating and neurodegenerative diseases1,2,3,4,5,6, but the pathways that control these responses remain unclear. Here we define a population of inflammatory group3 innate lymphoid cells (ILC3s) that infiltrate the CNS in a mouse model of multiple sclerosis. These ILC3s are derived from the circulation, localize in proximity to infiltrating T cells in the CNS, function as antigen-presenting cells that restimulate myelin-specific T cells, and are increased in individuals with multiple sclerosis. Notably, antigen presentation by inflammatory ILC3s is required to promote T cell responses in the CNS and the development of multiple-sclerosis-like disease in mouse models. By contrast, conventional and tissue-resident ILC3s in the periphery do not appear to contribute to disease induction, but instead limit autoimmune T cell responses and prevent multiple-sclerosis-like disease when experimentally targeted to present myelin antigen. Collectively, our data define a population of inflammatory ILC3s that is essential for directly promoting T-cell-dependent neuroinflammation in the CNS and reveal the potential of harnessing peripheral tissue-resident ILC3s for the prevention of autoimmune disease.

DOI: 10.1038/s41586-021-04136-4

Source: https://www.nature.com/articles/s41586-021-04136-4

Nature：《自然》，创刊于1869年。隶属于施普林格·自然出版集团，最新IF：69.504
官方网址：http://www.nature.com/
投稿链接：http://www.nature.com/authors/submit_manuscript.html