A T Cell Suppressive Circuitry Mediated by CD39 and Regulated by ShcC/Rai Is Induced in Astrocytes by Encephalitogenic T Cells.
Animals
Antigens, CD
/ metabolism
Apyrase
/ metabolism
Astrocytes
/ immunology
CD4-Positive T-Lymphocytes
/ immunology
CD8-Positive T-Lymphocytes
/ immunology
CTLA-4 Antigen
/ metabolism
Cell Proliferation
/ genetics
Cells, Cultured
Central Nervous System
/ immunology
Encephalomyelitis, Autoimmune, Experimental
/ immunology
Female
Lymphocyte Activation
/ immunology
Mice
Mice, Inbred C57BL
Mice, Knockout
Src Homology 2 Domain-Containing, Transforming Protein 3
/ genetics
ATP-degrading enzyme
EAE
T cell signaling
astrocyte
molecular adaptor
neuroinflammation
Journal
Frontiers in immunology
ISSN: 1664-3224
Titre abrégé: Front Immunol
Pays: Switzerland
ID NLM: 101560960
Informations de publication
Date de publication:
2019
2019
Historique:
received:
21
12
2018
accepted:
23
04
2019
entrez:
29
5
2019
pubmed:
28
5
2019
medline:
2
6
2020
Statut:
epublish
Résumé
Multiple sclerosis is an autoimmune disease caused by autoreactive immune cell infiltration into the central nervous system leading to inflammation, demyelination, and neuronal loss. While myelin-reactive Th1 and Th17 are centrally implicated in multiple sclerosis pathogenesis, the local CNS microenvironment, which is shaped by both infiltrated immune cells and central nervous system resident cells, has emerged a key player in disease onset and progression. We have recently demonstrated that ShcC/Rai is as a novel astrocytic adaptor whose loss in mice protects from experimental autoimmune encephalomyelitis. Here, we have explored the mechanisms that underlie the ability of Rai
Identifiants
pubmed: 31134091
doi: 10.3389/fimmu.2019.01041
pmc: PMC6524536
doi:
Substances chimiques
Antigens, CD
0
CTLA-4 Antigen
0
Shc3 protein, mouse
0
Src Homology 2 Domain-Containing, Transforming Protein 3
0
Apyrase
EC 3.6.1.5
CD39 antigen
EC 3.6.1.5
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
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