Group 2 innate lymphoid cells resolve neuroinflammation following cerebral ischaemia  

作　　者：Pei Zheng Yuwhen Xiu Zhili Chen Meng Yuan Yan Li Ningning Wang Bohao Zhang Xin Zhao Minshu Li Qiang Liu Fu-Dong Shi Wei-Na Jin 

机构地区：[1]Center for Neurological Diseases,China National Clinical Research Center for Neurological Diseases,Beijing Tiantan Hospital,Capital Medical University,Beijing,China [2]Department of Neurology,Tianjin Medical University General Hospital,Tianjin,China [3]Department of Neurology,The Third Affiliated Hospital of Zhengzhou University,Zhengzhou,Henan,China

出　　处：《Stroke & Vascular Neurology》2023年第5期424-434,共11页卒中与血管神经病学（英文）

基　　金：in part,by the National Natural Science Foundation of China(82071327,81971094,81771274).

摘　　要：Background Acute brain ischaemia elicits pronounced inflammation,which aggravates neural injury.However,the mechanisms governing the resolution of acute neuroinflammation remain poorly understood.In contrast to regulatory T and B cells,group 2 innate lymphoid cells(ILC2s)are immunoregulatory cells that can be swiftly mobilised without antigen presentation;whether and how these ILC2s participate in central nervous system inflammation following brain ischaemia is still unknown.Methods Leveraging brain tissues from patients who had an ischaemic stroke and a mouse model of focal ischaemia,we characterised the presence and cytokine release of brain-infiltrating ILC2s.The impact of ILC2s on neural injury was evaluated through antibody depletion and ILC2 adoptive transfer experiments.Using Rag2−/−γc−/−mice receiving passive transfer of IL-4−/−ILC2s,we further assessed the contribution of interleukin(IL)-4,produced by ILC2s,in ischaemic brain injury.Results We demonstrate that ILC2s accumulate in the areas surrounding the infarct in brain tissues of patients with cerebral ischaemia,as well as in mice subjected to focal cerebral ischaemia.Oligodendrocytes were a major source of IL-33,which contributed to ILC2s mobilisation.Adoptive transfer and expansion of ILC2s reduced brain infarction.Importantly,brain-infiltrating ILC2s reduced the magnitude of stroke injury severity through the production of IL-4.Conclusions Our findings revealed that brain ischaemia mobilises ILC2s to curb neuroinflammation and brain injury,expanding the current understanding of inflammatory networks following stroke.

关 键 词：INFLAMMATION CEREBRAL LYMPHOID 

分 类 号：R743.3[医药卫生—神经病学与精神病学]