Transcription cofactor GRIP1 differentially affects myeloid cell-driven neuroinflammation and response to IFN-β therapy.
Journal
The Journal of experimental medicine
ISSN: 1540-9538
Titre abrégé: J Exp Med
Pays: United States
ID NLM: 2985109R
Informations de publication
Date de publication:
04 01 2021
04 01 2021
Historique:
received:
20
12
2019
revised:
29
07
2020
accepted:
04
09
2020
entrez:
12
10
2020
pubmed:
13
10
2020
medline:
31
8
2021
Statut:
ppublish
Résumé
Macrophages (MФ) and microglia (MG) are critical in the pathogenesis of multiple sclerosis (MS) and its mouse model, experimental autoimmune encephalomyelitis (EAE). Glucocorticoids (GCs) and interferon β (IFN-β) are frontline treatments for MS, and disrupting each pathway in mice aggravates EAE. Glucocorticoid receptor-interacting protein 1 (GRIP1) facilitates both GR and type I IFN transcriptional actions; hence, we evaluated the role of GRIP1 in neuroinflammation. Surprisingly, myeloid cell-specific loss of GRIP1 dramatically reduced EAE severity, immune cell infiltration of the CNS, and MG activation and demyelination specifically during the neuroinflammatory phase of the disease, yet also blunted therapeutic properties of IFN-β. MФ/MG transcriptome analyses at the bulk and single-cell levels revealed that GRIP1 deletion attenuated nuclear receptor, inflammatory and, interestingly, type I IFN pathways and promoted the persistence of a homeostatic MG signature. Together, these results uncover the multifaceted function of type I IFN in MS/EAE pathogenesis and therapy, and an unexpectedly permissive role of myeloid cell GRIP1 in neuroinflammation.
Identifiants
pubmed: 33045064
pii: 211456
doi: 10.1084/jem.20192386
pmc: PMC7555412
pii:
doi:
Substances chimiques
Ncoa2 protein, mouse
0
Nuclear Receptor Coactivator 2
0
Interferon-beta
77238-31-4
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : NIAID NIH HHS
ID : R01 AI148129
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK099087
Pays : United States
Organisme : NINDS NIH HHS
ID : R21 NS110520
Pays : United States
Organisme : NIAMS NIH HHS
ID : T32 AR007281
Pays : United States
Commentaires et corrections
Type : ErratumIn
Informations de copyright
© 2020 Mimouna et al.
Déclaration de conflit d'intérêts
Disclosures: The authors declare no competing interests exist.
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