scholarly journals Paeoniflorin Ameliorates Experimental Autoimmune Encephalomyelitis via Inhibition of Dendritic Cell Function and Th17 Cell Differentiation

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Han Zhang ◽  
Yuanyuan Qi ◽  
Yuanyang Yuan ◽  
Li Cai ◽  
Haiyan Xu ◽  
...  
Keyword(s):  
Cell Differentiation ◽  
Dendritic Cell ◽  
Experimental Autoimmune Encephalomyelitis ◽  
Th17 Cell ◽  
Cell Function ◽  
Dendritic Cell Function ◽  
Autoimmune Encephalomyelitis ◽  
Th17 Cell Differentiation ◽  
Experimental Autoimmune

scholarly journals Silybin Alleviates Experimental Autoimmune Encephalomyelitis by Suppressing Dendritic Cell Activation and Th17 Cell Differentiation

2021 ◽  
Vol 12 ◽  
Author(s):  
Huan-Li Yang ◽  
Xiao-Wu Shi
Keyword(s):  
Cell Differentiation ◽  
Dendritic Cell ◽  
Experimental Autoimmune Encephalomyelitis ◽  
Th17 Cell ◽  
Cell Activation ◽  
Flavonoid Compound ◽  
Dendritic Cell Activation ◽  
Autoimmune Encephalomyelitis ◽  
Th17 Cell Differentiation ◽  
Experimental Autoimmune

Silybin, a peculiar flavonoid compound derived from the fruit and seeds of Silybum marianum, exhibits strong anti-inflammatory activities. In the present study, we found that silybin effectively alleviated experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS), via inhibition of dendritic cell (DC) activation and Th17 cell differentiation. Silybin treatment greatly ameliorated the disease severity and significantly declined inflammation and demyelination of the central nervous system (CNS) of EAE mice. Consistent with the disease development, silybin-treated bone marrow-derived DCs (BM-DCs) exhibited reduced costimulatory molecules (e.g., CD80 and CD86) and MHC II expression. These results demonstrated the distinguished bioactivity of silybin for suppressing DC activation, inhibiting pathogenic Th17 inflammatory cell responses, and, eventually, alleviating EAE severity. Taken together, our results show that silybin has high potential for the development of a novel therapeutic agent for the treatment of autoimmune diseases such as MS.

scholarly journals RGC-32 promotes Th17 cell differentiation and enhances experimental autoimmune encephalomyelitis

Immunobiology ◽  
2016 ◽  
Vol 221 (10) ◽  
pp. 1173
Author(s):  
Violeta Rus ◽  
Vinh Nguyen ◽  
Alexandru Tatomir ◽  
Dallas Boodhoo ◽  
Armugam P. Mekala ◽  
...  
Keyword(s):  
Cell Differentiation ◽  
Experimental Autoimmune Encephalomyelitis ◽  
Th17 Cell ◽  
Autoimmune Encephalomyelitis ◽  
Th17 Cell Differentiation ◽  
Experimental Autoimmune

scholarly journals RGC-32 Promotes Th17 Cell Differentiation and Enhances Experimental Autoimmune Encephalomyelitis

2017 ◽  
Vol 198 (10) ◽  
pp. 3869-3877 ◽  
Author(s):  
Violeta Rus ◽  
Vinh Nguyen ◽  
Alexandru Tatomir ◽  
Jason R. Lees ◽  
Armugam P. Mekala ◽  
...  
Keyword(s):  
Cell Differentiation ◽  
Experimental Autoimmune Encephalomyelitis ◽  
Th17 Cell ◽  
Autoimmune Encephalomyelitis ◽  
Th17 Cell Differentiation ◽  
Experimental Autoimmune

scholarly journals SKI Expression Suppresses Pathogenic Th17 Cell Response and Mitigates Experimental Autoimmune Encephalomyelitis

2021 ◽  
Vol 12 ◽  
Author(s):  
Ping Li ◽  
Zengli Guo ◽  
Yisong Y. Wan
Keyword(s):  
Cell Differentiation ◽  
Experimental Autoimmune Encephalomyelitis ◽  
Th17 Cell ◽  
Th17 Cells ◽  
Transforming Growth Factor ◽  
Ectopic Expression ◽  
Transfer Model ◽  
Autoimmune Encephalomyelitis ◽  
Th17 Cell Differentiation ◽  
Experimental Autoimmune

Pathogenic Th17 cells are critically involved in many autoimmune diseases, while non-pathogenic Th17 cells are more immune regulatory. Understanding the mechanisms of the induction and maintenance of pathogenic Th17 cells will benefit the development of therapeutic treatments of related diseases. We have shown that the transforming growth factor-β (TGFβ) induced SKI degradation and dissociation from Smad4 complex is a prerequisite for TGFβ-induced Th17 cell differentiation. However, it is unclear whether and how SKI regulates pathogenic Th17 differentiation, which does not require TGFβ cytokine. Here we showed that SKI expression was downregulated during pathogenic Th17 cell differentiation and the ectopic expression of SKI abrogated the differentiation of pathogenic Th17 cells. Functionally, using a knock-in mouse model, we found ectopic SKI expression specifically in T cells prevented myelin oligodendrocyte glycoprotein peptide (MOG33–55) induced experimental autoimmune encephalomyelitis (EAE), an animal model of human multiple sclerosis. We further revealed that induced SKI expression in already differentiated pathogenic Th17 cells reduced the maintenance of Th17 program and ameliorated EAE in an adoptive T cell transfer model. Therefore, our study provides valuable insights of targeting SKI to modulate pathogenic Th17 cell function and treat Th17-related diseases.

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