2. Academic Validation
  3. The ribosomal S6 kinase inhibitor BI-D1870 ameliorated experimental autoimmune encephalomyelitis in mice

The ribosomal S6 kinase inhibitor BI-D1870 ameliorated experimental autoimmune encephalomyelitis in mice

  • Immunobiology. 2016 Feb;221(2):188-92. doi: 10.1016/j.imbio.2015.09.008.
Ichiro Takada 1,  Yoshiko Yogiashi 2,  Makoto Makishima 3
Affiliations

Affiliations

  • 1 Division of Biochemistry, Department of Biomedical Sciences, School of Medicine, Nihon University, Itabashi-ku, Tokyo 173-8610, Japan; School of Medicine, Keio University, Shinjuku-ku, Tokyo 160-8582, Japan. Electronic address: [email protected].
  • 2 School of Medicine, Keio University, Shinjuku-ku, Tokyo 160-8582, Japan.
  • 3 Division of Biochemistry, Department of Biomedical Sciences, School of Medicine, Nihon University, Itabashi-ku, Tokyo 173-8610, Japan.
PMID: 26386981 DOI: 10.1016/j.imbio.2015.09.008
Abstract

Multiple sclerosis (MS) is an autoimmune demyelinating disease of the central nervous system (CNS) caused by the infiltration of TH1 and TH17 cells into the CNS. Ribosomal S6 kinase 2 (RSK2; RPS6KA3) regulates TH17 differentiation by attenuating RORγt transcriptional activities and IL-17A production. The pan-RSK inhibitor BI-D1870 also inhibits TH17 differentiation, but the effect of BI-D1870 in vivo remains unclear. Here, we generated mice with experimental autoimmune encephalomyelitis (EAE) and treated them with BI-D1870. BI-D1870 administration protected mice from EAE by reducing the infiltration of TH1 and TH17 cells into the CNS and decreasing mRNA levels of CCR6 in TH17 cells. These results suggest that RSK inhibition is a promising strategy for the treatment of MS.

Keywords

RORgt; RSK; Th17 cell.

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