NOD2 deficiency protects mice from the development of adoptive transfer colitis through the induction of regulatory T cells expressing forkhead box P3.
Adoptive transfer colitis
NOD2
Regulatory T cell
TGF-β1
Journal
Biochemical and biophysical research communications
ISSN: 1090-2104
Titre abrégé: Biochem Biophys Res Commun
Pays: United States
ID NLM: 0372516
Informations de publication
Date de publication:
03 09 2021
03 09 2021
Historique:
received:
12
06
2021
accepted:
19
06
2021
pubmed:
30
6
2021
medline:
20
11
2021
entrez:
29
6
2021
Statut:
ppublish
Résumé
Nucleotide-binding oligomerization domain 2 (NOD2) is an intracellular receptor for muramyl dipeptide derived from the intestinal microbiota. Loss-of-function mutations in Nod2 are associated with the development of Crohn's disease, suggesting that NOD2 signaling plays critical roles in the maintenance of intestinal immune homeostasis. Although NOD2 activation prevents the development of short-term experimental colitis, it remains unknown whether the sensitivity to long-term experimental colitis is influenced by NOD2. In this study, we explored the roles played by NOD2 in the development of long-term adoptive transfer colitis. Unexpectedly, we found that Rag1
Identifiants
pubmed: 34186435
pii: S0006-291X(21)00990-6
doi: 10.1016/j.bbrc.2021.06.068
pii:
doi:
Substances chimiques
Forkhead Transcription Factors
0
Foxp3 protein, mouse
0
Nod2 Signaling Adaptor Protein
0
Nod2 protein, mouse
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
55-61Informations de copyright
Copyright © 2021 Elsevier Inc. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have influenced the work reported in this paper.