HMGB1
实验性自身免疫性脑脊髓炎
免疫学
体外
神经免疫学
中枢神经系统
脑脊髓炎
条件基因敲除
白细胞介素
生物
化学
多发性硬化
神经科学
免疫系统
炎症
细胞因子
表型
生物化学
基因
作者
Mengya Jiao,Yan Sun,Junyu Shi,Na Zhang,Xuhuan Tang,Anqi Fan,Shiwang Liu,Chan Dai,Zhi‐Gang Qian,Feng Zhang,Chenchen Wang,Huoying Chen,Zheng Fang
标识
DOI:10.1016/j.intimp.2023.110653
摘要
Interleukin-33 (IL-33) and high mobility group box 1 (HMGB1) have been reported to play crucial and distinct roles in experimental autoimmune encephalomyelitis (EAE). However, little is known about their interaction in the progression of EAE. In this study, the dynamic expression and release of IL-33 and HMGB1 in different stages of EAE in vivo, and their interaction in vitro were explored. We found that HMGB1 was dominant in pre-onset stage of EAE, while IL-33 was dominant in peak stage. Moreover, both blockade of extracellular HMGB1 in the central nervous system (CNS) and conditional knockout of HMGB1 in astrocytes decreased IL-33 release. HMGB1 promoted the release of IL-33, while IL-33 reduced the release of HMGB1 from primary astrocytes in vitro. Taken together, IL-33 and HMGB1 in the CNS jointly participate in the EAE progression and the inhibitory effect of IL-33 on HMGB1 may be involved in the self-limiting of EAE.
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