Eriocalyxin B ameliorates experimental autoimmune encephalomyelitis by suppressing Th1 and Th17 cells

• Published in: Proceedings of the National Academy of Sciences - PNAS 2013-02, Vol.110 (6), p.2258-2263
• Main Authors: 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
• Format: Article
• Language: English
• Subjects: Adoptive Transfer; Animals; Autoimmune diseases; Autoimmunity - drug effects; Biological Sciences; Cells; Cellular differentiation; Central nervous system diseases; Cultured cells; Cytokines; Diterpenes - pharmacology; Encephalomyelitis, Autoimmune, Experimental - drug therapy; Encephalomyelitis, Autoimmune, Experimental - immunology; Encephalomyelitis, Autoimmune, Experimental - metabolism; Encephalomyelitis, Autoimmune, Experimental - pathology; Female; Glycoproteins; Immunosuppressive Agents - pharmacology; Inflammation; Lymphocytes; Medical treatment; Medicine, Chinese Traditional; Mice; Mice, Inbred C57BL; Multiple sclerosis; Nervous system diseases; NF-kappa B - metabolism; Pharmaceuticals; Phosphorylation; Reactive Oxygen Species - metabolism; Signal Transduction - drug effects; Signal Transduction - immunology; Splenocytes; T lymphocytes; Th1 Cells - drug effects; Th1 Cells - immunology; Th17 Cells - drug effects; Th17 Cells - immunology; Vehicles
• ISSN: 0027-8424; 1091-6490
• DOI: 10.1073/pnas.1222426110

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 ah) 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.