IL-3 receptor signalling suppresses chronic intestinal inflammation by controlling mechanobiology and tissue egress of regulatory T cells.
CYTOKINES
INFLAMMATORY BOWEL DISEASE
INTESTINAL T CELLS
Journal
Gut
ISSN: 1468-3288
Titre abrégé: Gut
Pays: England
ID NLM: 2985108R
Informations de publication
Date de publication:
11 2023
11 2023
Historique:
received:
03
03
2023
accepted:
16
06
2023
medline:
23
10
2023
pubmed:
5
8
2023
entrez:
4
8
2023
Statut:
ppublish
Résumé
IL-3 has been reported to be involved in various inflammatory disorders, but its role in inflammatory bowel disease (IBD) has not been addressed so far. Here, we determined IL-3 expression in samples from patients with IBD and studied the impact of
Identifiants
pubmed: 37541770
pii: gutjnl-2023-329818
doi: 10.1136/gutjnl-2023-329818
pmc: PMC10579496
doi:
Substances chimiques
Receptors, Interleukin-3
0
Interleukin-3
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
2081-2094Informations de copyright
© Author(s) (or their employer(s)) 2023. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.
Déclaration de conflit d'intérêts
Competing interests: MFN has served as an advisor for Pentax, Giuliani, MSD, AbbVie, Janssen, Takeda and Boehringer. SZ received honoraria from Takeda, Roche, Galapagos, Ferring, Falk, Lilly and Janssen. MFN and SZ received research support from Takeda, Shire (a part of Takeda) and Roche. JG and MK are co-founders of Rivercyte GmbH, a company that develops biomedical applications for real-time deformability cytometry. The other authors declare no conflicts of interest.
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