Interleukin-33 deficiency exacerbated experimental autoimmune encephalomyelitis with an influence on immune cells and glia cells.

Yifan Xiao,Lin Lai,Huoying Chen,Junyu Shi,FanFan Zeng,Jun Li, Huiting Feng,Jie Mao,Feng Zhang, Naming Wu,Yong Xu,Zheng Tan,Feili Gong,Fang Zheng

Molecular Immunology（2018）

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摘要

•IL-33 knockout aggravates the development of EAE.•IL-33 knockout inhibits Th2, NK cells and promotes Th1/Th17 cells.•IL-33 knockout promotes iNOS-producing microglia/macrophages and CD11C+CD11B+ DCs.•IL-33 suppresses the activation of astrocytes and the release of MCP-1/CCL2, TNF-α from them.•IL-33 suppresses TNF-α releasing from primary microglia.

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关键词

BBB,CNS,CSF,DCs,EAE,GFAP,IFN,IL,IVIG,ILC2s,MS,MCP-1/CCL2,NeuN,RA,SLE,ST2,TNF-α,Th,Tc,Tregs

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