IL-11 antagonist suppresses Th17 cell-mediated neuroinflammation and demyelination in a mouse model of relapsing-remitting multiple sclerosis.

Published

Journal Article

IL-11 induced differentiation and expansion of Th17 cells in patients with early relapsing-remitting multiple sclerosis (RRMS). In mice with relapsing-remitting experimental autoimmune encephalomyelitis (RREAE), IL-11 exacerbated disease, induced demyelination in the central nervous system (CNS), increased the percentage of IL-17A+CD4+ Th17 cells in the CNS in the early acute phase, and up-regulated serum IL-17A levels and the percentage of IL-17A+CD4+ Th17 cells in lymph nodes, and IFN-γ+CD4+ T cells in spinal cord in the RR phase. IL-11 antagonist suppressed RREAE disease activities, inhibited IL-17A+CD4+ cell infiltration and demyelination in the CNS, and decreased the percentage of IL-17A+CD4+ T cells in peripheral blood mononuclear cells and ICAM1+CD4+ T cells in brain and SC. Diffusion Tensor Imaging indicated that IL-11 antagonist inhibited demyelination in several brain regions. We conclude that by suppressing Th17 cell-mediated neuroinflammation and demyelination, IL-11 antagonist can be further studied as a potential selective and early therapy for RRMS.

Full Text

Cited Authors

  • Zhang, X; Kiapour, N; Kapoor, S; Merrill, JR; Xia, Y; Ban, W; Cohen, SM; Midkiff, BR; Jewells, V; Shih, Y-YI; Markovic-Plese, S

Published Date

  • December 2018

Published In

Volume / Issue

  • 197 /

Start / End Page

  • 45 - 53

PubMed ID

  • 30149119

Pubmed Central ID

  • 30149119

Electronic International Standard Serial Number (EISSN)

  • 1521-7035

Digital Object Identifier (DOI)

  • 10.1016/j.clim.2018.08.006

Language

  • eng

Conference Location

  • United States