Helmholtz Gemeinschaft

Search
Browse
Statistics
Feeds

BTK inhibition limits microglia‑perpetuated CNS inflammation and promotes myelin repair

[img]
Preview
PDF (Original Article) - Requires a PDF viewer such as GSview, Xpdf or Adobe Acrobat Reader
10MB
[img] Other (Supplementary Information)
18MB

Item Type:Article
Title:BTK inhibition limits microglia‑perpetuated CNS inflammation and promotes myelin repair
Creators Name:Geladaris, A. and Torke, S. and Saberi, D. and Alankus, Y.B. and Streit, F. and Zechel, S. and Stadelmann-Nessler, C. and Fischer, A. and Boschert, U. and Häusler, D. and Weber, M.S.
Abstract:In multiple sclerosis (MS), persisting disability can occur independent of relapse activity or development of new central nervous system (CNS) inflammatory lesions, termed chronic progression. This process occurs early and it is mostly driven by cells within the CNS. One promising strategy to control progression of MS is the inhibition of the enzyme Bruton's tyrosine kinase (BTK), which is centrally involved in the activation of both B cells and myeloid cells, such as macrophages and microglia. The benefit of BTK inhibition by evobrutinib was shown as we observed reduced pro-inflammatory activation of microglia when treating chronic experimental autoimmune encephalomyelitis (EAE) or following the adoptive transfer of activated T cells. Additionally, in a model of toxic demyelination, evobrutinib-mediated BTK inhibition promoted the clearance of myelin debris by microglia, leading to an accelerated remyelination. These findings highlight that BTK inhibition has the potential to counteract underlying chronic progression of MS.
Keywords:Multiple Sclerosis, Progression, Microglia, BTK Inhibition, Animals, Mice
Source:Acta Neuropathologica
ISSN:0001-6322
Publisher:Springer
Volume:147
Number:1
Page Range:75
Date:24 April 2024
Official Publication:https://doi.org/10.1007/s00401-024-02730-0
PubMed:View item in PubMed

Repository Staff Only: item control page

Downloads

Downloads per month over past year

Open Access
MDC Library