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

Authors: 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

Published In Clin Immunol, (2018 12)

Abstract: 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.

PubMed ID: 30149119 Exiting the NIEHS site

MeSH Terms: Animals; Brain/diagnostic imaging*; Brain/immunology; Diffusion Tensor Imaging; Encephalomyelitis, Autoimmune, Experimental/immunology*; Inflammation; Interleukin-11 Receptor alpha Subunit; Interleukin-11/antagonists & inhibitors*; Interleukin-11/immunology; Leukocytes, Mononuclear; Mice; Multiple Sclerosis, Relapsing-Remitting; Recombinant Fusion Proteins; Spinal Cord/diagnostic imaging*; Spinal Cord/immunology; Th17 Cells/immunology*

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