中国科学技术大学占成课题组发现，空腹激活的延髓腹外侧神经元能调节T细胞归巢并抑制小鼠的自身免疫性疾病。这一研究成果于2024年1月5日在线发表在国际学术期刊《自然—神经科学》上。

研究人员报告了小鼠在空腹期间延髓腹外侧（VLM）的儿茶酚胺能（CA）神经元被激活的情况，并证明了这些CA神经元的活性会影响T细胞的分布以及实验性自身免疫性脑脊髓炎（EAE）模型中自身免疫性疾病的发展。去除VLM CA神经元在很大程度上逆转了空腹介导的T细胞重新分布。这些神经元的激活以CXCR4/CXCL12轴依赖的方式促使T细胞向骨髓归巢，这可能是由刺激皮质酮分泌的神经回路介导的。

与空腹类似，持续激活VLM CA神经元可抑制自身免疫小鼠模型中T细胞的活化、增殖、分化和细胞因子的产生，并大大缓解疾病症状。总之，这项研究证明了神经元对炎症和T细胞分布的控制，并提示了空腹介导的免疫调节的神经机制。

据介绍，空腹会明显影响免疫细胞的分布和功能，并产生强大的免疫抑制作用。然而，空腹调节免疫的机制仍然模糊不清。

附：英文原文

Title: Fasting-activated ventrolateral medulla neurons regulate T cell homing and suppress autoimmune disease in mice

Author: Wang, Liang, Cheng, Mingxiu, Wang, Yuchen, Chen, Jing, Xie, Famin, Huang, Li-Hao, Zhan, Cheng

Issue&Volume: 2024-01-05

Abstract: Dietary fasting markedly influences the distribution and function of immune cells and exerts potent immunosuppressive effects. However, the mechanisms through which fasting regulates immunity remain obscure. Here we report that catecholaminergic (CA) neurons in the ventrolateral medulla (VLM) are activated during fasting in mice, and we demonstrate that the activity of these CA neurons impacts the distribution of T cells and the development of autoimmune disease in an experimental autoimmune encephalomyelitis (EAE) model. Ablation of VLM CA neurons largely reversed fasting-mediated T cell redistribution. Activation of these neurons drove T cell homing to bone marrow in a CXCR4/CXCL12 axis-dependent manner, which may be mediated by a neural circuit that stimulates corticosterone secretion. Similar to fasting, the continuous activation of VLM CA neurons suppressed T cell activation, proliferation, differentiation and cytokine production in autoimmune mouse models and substantially alleviated disease symptoms. Collectively, our study demonstrates neuronal control of inflammation and T cell distribution, suggesting a neural mechanism underlying fasting-mediated immune regulation.

DOI: 10.1038/s41593-023-01543-w

Source: https://www.nature.com/articles/s41593-023-01543-w