白介素-33 和高迁移率族蛋白 B1 通过相互调节来调控实验性自身免疫性脑脊髓炎的进展。
IL-33 and HMGB1 modulate the progression of EAE via oppositely regulating each other.
机构信息
Department of Immunology, School of Basic Medicine, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonostic Infectious Disease, Huazhong University of Science and Technology, Wuhan, 430030, Hubei, China.
Wuhan Institute for Neuroscience and Neuroengineering, South-Central Minzu University, Wuhan 430074, China; College of Life Sciences, South-Central Minzu University, Wuhan 430074, China.
出版信息
Int Immunopharmacol. 2023 Sep;122:110653. doi: 10.1016/j.intimp.2023.110653. Epub 2023 Jul 18.
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.
白细胞介素-33（IL-33）和高迁移率族蛋白 B1（HMGB1）已被报道在实验性自身免疫性脑脊髓炎（EAE）中发挥关键且不同的作用。然而，它们在 EAE 进展中的相互作用知之甚少。在这项研究中，我们探讨了体内 EAE 不同阶段中 IL-33 和 HMGB1 的动态表达和释放，以及它们在体外的相互作用。我们发现 HMGB1 在 EAE 的前驱期占主导地位，而 IL-33 在高峰期占主导地位。此外，阻断中枢神经系统（CNS）中的细胞外 HMGB1 和条件性敲除星形胶质细胞中的 HMGB1 均可减少 IL-33 的释放。HMGB1 促进 IL-33 的释放，而 IL-33 减少体外原代星形胶质细胞中 HMGB1 的释放。综上所述，CNS 中的 IL-33 和 HMGB1 共同参与 EAE 的进展，而 IL-33 对 HMGB1 的抑制作用可能涉及 EAE 的自限性。
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