IL-11 antagonist suppresses Th17 cell-mediated neuroinflammation and demyelination in a mouse model of relapsing-remitting multiple sclerosis
Copyright © 2018 Elsevier Inc. All rights reserved.
Publié dans: | Clinical immunology (Orlando, Fla.). - 1999. - 197(2018) vom: 08. Dez., Seite 45-53 |
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Auteur principal: | |
Autres auteurs: | , , , , , , , , , |
Format: | Article en ligne |
Langue: | English |
Publié: |
2018
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Accès à la collection: | Clinical immunology (Orlando, Fla.) |
Sujets: | Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Demyelination Diffusion Tensor Imaging Experimental autoimmune encephalomyelitis IL-11 Multiple sclerosis Th17 cells Interleukin-11 plus... |
Résumé: | Copyright © 2018 Elsevier Inc. All rights reserved. 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 |
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Description: | Date Completed 07.10.2019 Date Revised 28.10.2022 published: Print-Electronic Citation Status MEDLINE |
ISSN: | 1521-7035 |
DOI: | 10.1016/j.clim.2018.08.006 |