Ponesimod modulates the Th1/Th17/Treg cell balance and ameliorates disease in experimental autoimmune encephalomyelitis

  • J Neuroimmunol. 2021 Jul 15:356:577583. doi: 10.1016/j.jneuroim.2021.577583.
Huiqing Hou  1 ,  Yafei Sun  1 ,  Jun Miao  2 ,  Mengying Gao  3 ,  Li Guo  1 ,  Xiujuan Song  4
Affiliations
  • 1. Department of Neurology, Key Laboratory of Hebei Neurology, the Second Hospital of Hebei Medical University, Shijiazhuang 050000, Hebei, China.
  • 2. Department of Dermatology, North China Petroleum Bureau General Hospital of Hebei Medical University, Renqiu 062552, Hebei, China.
  • 3. Emergency Department, the Second Hospital of Hebei Medical University, Shijiazhuang 050000, Hebei, China.
  • 4. Department of Neurology, Key Laboratory of Hebei Neurology, the Second Hospital of Hebei Medical University, Shijiazhuang 050000, Hebei, China. Electronic address: [email protected].
PMID: 33940233 DOI: 10.1016/j.jneuroim.2021.577583
Abstract

Sphingosine-1-phosphate receptor 1 (S1P1) plays an important role in autoimmune disease. Here, we evaluated whether ponesimod, an S1P1 modulator, affects inflammation in experimental autoimmune encephalomyelitis (EAE) and investigated Th1/Th2/Th17/Treg cell subsets. Ponesimod treatment ameliorated EAE and alleviated inflammatory infiltration. Compared with untreated EAE, ponesimod-treated mice had lower Th1 and Th17 cell numbers and higher Treg cell numbers; their IFN-γ, T-bet, IL-17, and RORγt levels as well as their pmTOR/mTOR ratio were diminished, while their TGF-β and Foxp3 levels were enhanced. These results suggest that ponesimod modulates the Th1/Th17/Treg balance and regulates the mTOR pathway.

Keywords
Experimental autoimmune encephalomyelitis; Multiple sclerosis; Ponesimod; Sphingosine-1-phosphate receptor; Th1; Th17; Treg.
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