Microglial autophagy-associated phagocytosis is essential for recovery from neuroinflammation.
Animals
Autophagy
/ immunology
Autophagy-Related Protein 7
/ deficiency
Autophagy-Related Protein-1 Homolog
/ deficiency
Brain
/ cytology
Cells, Cultured
Encephalomyelitis, Autoimmune, Experimental
/ immunology
Female
Humans
Male
Mice
Mice, Knockout
Microglia
/ immunology
Multiple Sclerosis
/ immunology
Myelin Sheath
/ metabolism
Phagocytosis
/ immunology
Primary Cell Culture
Spinal Cord
/ cytology
Journal
Science immunology
ISSN: 2470-9468
Titre abrégé: Sci Immunol
Pays: United States
ID NLM: 101688624
Informations de publication
Date de publication:
16 10 2020
16 10 2020
Historique:
received:
28
02
2020
accepted:
24
09
2020
entrez:
17
10
2020
pubmed:
18
10
2020
medline:
21
9
2021
Statut:
ppublish
Résumé
Multiple sclerosis (MS) is a leading cause of incurable progressive disability in young adults caused by inflammation and neurodegeneration in the central nervous system (CNS). The capacity of microglia to clear tissue debris is essential for maintaining and restoring CNS homeostasis. This capacity diminishes with age, and age strongly associates with MS disease progression, although the underlying mechanisms are still largely elusive. Here, we demonstrate that the recovery from CNS inflammation in a murine model of MS is dependent on the ability of microglia to clear tissue debris. Microglia-specific deletion of the autophagy regulator
Identifiants
pubmed: 33067381
pii: 5/52/eabb5077
doi: 10.1126/sciimmunol.abb5077
pii:
doi:
Substances chimiques
Atg7 protein, mouse
0
Autophagy-Related Protein-1 Homolog
EC 2.7.11.1
Ulk1 protein, mouse
EC 2.7.11.1
Autophagy-Related Protein 7
EC 6.2.1.45
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Informations de copyright
Copyright © 2020 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works.