Asset Details
Do you wish to reserve the book?
CD40L protects against mouse hepatitis virus-induced neuroinflammatory demyelination
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?
CD40L protects against mouse hepatitis virus-induced neuroinflammatory demyelination
Do you wish to request the book?
CD40L protects against mouse hepatitis virus-induced neuroinflammatory demyelination
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
CD40L protects against mouse hepatitis virus-induced neuroinflammatory demyelination
2021
Overview
Neurotropic mouse hepatitis virus (MHV-A59/RSA59) infection in mice induces acute neuroinflammation due to direct neural cell dystrophy, which proceeds with demyelination with or without axonal loss, the pathological hallmarks of human neurological disease, Multiple sclerosis (MS). Recent studies in the RSA59-induced neuroinflammation model of MS showed a protective role of CNS-infiltrating CD4
+
T cells compared to their pathogenic role in the autoimmune model. The current study further investigated the molecular nexus between CD4
+
T cell-expressed CD40Ligand and microglia/macrophage-expressed CD40 using CD40L
-/-
mice. Results demonstrate CD40L expression in the CNS is modulated upon RSA59 infection. We show evidence that CD40L
-/-
mice are more susceptible to RSA59 induced disease due to reduced microglia/macrophage activation and significantly dampened effector CD4
+
T recruitment to the CNS on day 10 p.i. Additionally, CD40L
-/-
mice exhibited severe demyelination mediated by phagocytic microglia/macrophages, axonal loss, and persistent poliomyelitis during chronic infection, indicating CD40-CD40L as host-protective against RSA59-induced demyelination. This suggests a novel target in designing prophylaxis for virus-induced demyelination and axonal degeneration, in contrast to immunosuppression which holds only for autoimmune mechanisms of inflammatory demyelination.
Publisher
Public Library of Science,Public Library of Science (PLoS)
Subject
/ Brain
/ Coronavirus Infections - immunology
/ Coronavirus Infections - pathology
/ Medicine and Health Sciences
/ Mice
/ Nervous System Autoimmune Disease, Experimental - immunology
/ Nervous System Autoimmune Disease, Experimental - pathology
/ Nervous System Autoimmune Disease, Experimental - virology
/ Proteins
/ Research and Analysis Methods
/ Rodents
/ T cells
/ Viruses
