| Literature DB >> 30149119 |
Xin Zhang1, Nazanin Kiapour2, Sahil Kapoor2, Joseph R Merrill3, Yongjuan Xia4, Woomi Ban3, Stephanie M Cohen4, Bentley R Midkiff4, Valerie Jewells5, Yen-Yu I Shih6, Silva Markovic-Plese7.
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.Entities:
Keywords: Demyelination; Diffusion Tensor Imaging; Experimental autoimmune encephalomyelitis; IL-11; Multiple sclerosis; Th17 cells
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Year: 2018 PMID： 30149119 PMCID： PMC7953940 DOI： 10.1016/j.clim.2018.08.006
Source DB: PubMed Journal: Clin Immunol ISSN： 1521-6616 Impact factor: 3.969