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Eriocalyxin B ameliorates experimental autoimmune encephalomyelitis by suppressing Th1 and Th17 cells
- Lu, Ying, Chen, Bing, Song, Jun-Hong, Zhen, Tao, Wang, Bai-Yan, Li, Xin, Liu, Ping, Yang, Xin, Zhang, Qun-Ling, Xi, Xiao-Dong, Chen, Sheng-Di, Zuo, Jian-Ping, Chen, Zhu, Chen, Sai-Juan
- Proceedings of the National Academy of Sciences of the United States of America 2013 v.110 no.6 pp. 2258-2263
- CD4-positive T-lymphocytes, animal models, anti-inflammatory activity, antineoplastic activity, autoimmune diseases, cell differentiation, diterpenoids, encephalitis, glycoproteins, immune response, inflammation, myelin sheath, non-specific protein-tyrosine kinase, oligodendroglia, reactive oxygen species, sclerosis, signal transduction, spinal cord, transactivators, transcription factor NF-kappa B
- Eriocalyxin B (EriB), a diterpenoid isolated from Isodon eriocalyx , was previously reported to have antitumor effects via multiple pathways, and these pathways are related to immune responses. In this study, we demonstrated that EriB was efficacious in experimental autoimmune encephalomyelitis (EAE), an animal model for multiple sclerosis. Treatment with EriB led to amelioration of EAE, which correlated with reduced spinal cord inflammation and demyelination. EriB treatment abolished encephalitogenic T-cell responses to myelin oligodendrocyte glycoprotein in an adoptive transfer EAE model. The underlying mechanism of EriB-induced effects involved inhibition of T helper (Th) 1 and Th17 cell differentiation through Janus Kinase/Signal Transducer and Activator Of Transcription and Nuclear factor-κB signaling pathways as well as elevation of reactive oxygen species. These findings indicate that EriB exerts potent antiinflammatory effects through selective modulation of pathogenic Th1 and Th17 cells by targeting critical signaling pathways. The study provides insights into the role of EriB as a unique therapeutic agent for the treatment of autoimmune diseases.