Details

Autor(en) / Beteiligte

• Zhang, Xin
• Kiapour, Nazanin
• Kapoor, Sahil
• Merrill, Joseph R.
• Xia, Yongjuan
• Ban, Woomi
• Cohen, Stephanie M.
• Midkiff, Bentley R.
• Jewells, Valerie
• Shih, Yen-Yu I.
• Markovic-Plese, Silva

Titel

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

Ist Teil von

• Clinical immunology (Orlando, Fla.), 2018-12, Vol.197, p.45-53

Ort / Verlag

United States: Elsevier Inc

Erscheinungsjahr

2018

Quelle

MEDLINE

Beschreibungen/Notizen

• 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. •IL-11 exacerbates relapsing-remitting experimental autoimmune encephalomyelitis.•IL-11 induced Th17 cell-mediated neuroinflammation and demyelination in the CNS.•IL-11 antagonist suppresses relapsing-remitting experimental autoimmune encephalomyelitis.•IL-11 antagonist inhibits Th17 cell infiltration and demyelination in the CNS.