Asset Details
Do you wish to reserve the book?
BTK inhibition limits microglia-perpetuated CNS inflammation and promotes myelin repair
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
BTK inhibition limits microglia-perpetuated CNS inflammation and promotes myelin repair
Do you wish to request the book?
BTK inhibition limits microglia-perpetuated CNS inflammation and promotes myelin repair
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
BTK inhibition limits microglia-perpetuated CNS inflammation and promotes myelin repair
2024
Overview
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.
Publisher
Springer Berlin Heidelberg,Springer,Springer Nature B.V
Subject
/ Agammaglobulinaemia Tyrosine Kinase - antagonists & inhibitors
/ Agammaglobulinaemia Tyrosine Kinase - metabolism
/ Animals
/ B cells
/ Biphenyl Compounds - pharmacology
/ Encephalomyelitis, Autoimmune, Experimental - pathology
/ Enzymes
/ Experimental allergic encephalomyelitis
/ Female
/ Kinases
/ Medicine
/ Mice
/ Myelin
/ Peptides
/ Protein Kinase Inhibitors - pharmacology
/ Remyelination - drug effects
/ T cells
