STAT3 signaling in myeloid cells promotes pathogenic myelin-specific T cell differentiation and autoimmune demyelination.
Animals
CD11b Antigen
/ analysis
Cell Differentiation
Encephalomyelitis, Autoimmune, Experimental
/ genetics
Humans
Lymphocyte Activation
Mice
Mice, Inbred C57BL
Mice, Mutant Strains
Multiple Sclerosis
/ genetics
Myeloid Cells
/ immunology
STAT3 Transcription Factor
/ genetics
Single-Cell Analysis
T-Lymphocyte Subsets
/ immunology
Transcriptome
EAE
STAT3 signaling
T cell activation
multiple sclerosis
myeloid cells
Journal
Proceedings of the National Academy of Sciences of the United States of America
ISSN: 1091-6490
Titre abrégé: Proc Natl Acad Sci U S A
Pays: United States
ID NLM: 7505876
Informations de publication
Date de publication:
10 03 2020
10 03 2020
Historique:
pubmed:
26
2
2020
medline:
14
7
2020
entrez:
26
2
2020
Statut:
ppublish
Résumé
Multiple sclerosis (MS) is an autoimmune inflammatory demyelinating disease of the central nervous system. Dysregulation of STAT3, a transcription factor pivotal to various cellular processes including Th17 cell differentiation, has been implicated in MS. Here, we report that STAT3 is activated in infiltrating monocytic cells near active MS lesions and that activation of STAT3 in myeloid cells is essential for leukocyte infiltration, neuroinflammation, and demyelination in experimental autoimmune encephalomyelitis (EAE). Genetic disruption of
Identifiants
pubmed: 32094172
pii: 1913997117
doi: 10.1073/pnas.1913997117
pmc: PMC7071888
doi:
Substances chimiques
CD11b Antigen
0
STAT3 Transcription Factor
0
Stat3 protein, mouse
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Langues
eng
Sous-ensembles de citation
IM
Pagination
5430-5441Subventions
Organisme : NIDDK NIH HHS
ID : R01 DK098662
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK121805
Pays : United States
Organisme : NINDS NIH HHS
ID : R01 NS060017
Pays : United States
Informations de copyright
Copyright © 2020 the Author(s). Published by PNAS.
Déclaration de conflit d'intérêts
The authors declare no competing interest.
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