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.

Détails bibliographiques
Publié dans:Clinical immunology (Orlando, Fla.). - 1999. - 197(2018) vom: 08. Dez., Seite 45-53
Auteur principal: Zhang, Xin (Auteur)
Autres auteurs: 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
Format: Article en ligne
Langue:English
Publié: 2018
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... Interleukin-11 Receptor alpha Subunit Recombinant Fusion Proteins
Description
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
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