Activin A treated Th17 cells from mouse
Ontology highlight
ABSTRACT:
INSTRUMENT(S): Orbitrap Eclipse
ORGANISM(S): Mus Musculus (mouse)
TISSUE(S): T Cell
DISEASE(S): Multiple Sclerosis
SUBMITTER: 
Brett Lomenick
LAB HEAD: Spiros D. Garbis
PROVIDER: PXD017757 | Pride | 2020-05-18
REPOSITORIES: Pride
Publications
Activin-A limits Th17 pathogenicity and autoimmune neuroinflammation via CD39 and CD73 ectonucleotidases and Hif1-α-dependent pathways.
Morianos Ioannis I Trochoutsou Aikaterini I AI Papadopoulou Gina G Semitekolou Maria M Banos Aggelos A Konstantopoulos Dimitris D Manousopoulou Antigoni A Kapasa Maria M Wei Ping P Lomenick Brett B Belaidi Elise E Kalamatas Themis T Karageorgiou Klinta K Doskas Triantafyllos T Sallusto Federica F Pan Fan F Garbis Spiros D SD Quintana Francisco J FJ Xanthou Georgina G
Proceedings of the National Academy of Sciences of the United States of America 20200514 22
In multiple sclerosis (MS), Th17 cells are critical drivers of autoimmune central nervous system (CNS) inflammation and demyelination. Th17 cells exhibit functional heterogeneity fostering both pathogenic and nonpathogenic, tissue-protective functions. Still, the factors that control Th17 pathogenicity remain incompletely defined. Here, using experimental autoimmune encephalomyelitis, an established mouse MS model, we report that therapeutic administration of activin-A ameliorates disease severi ...[more]
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