XIAP restrains TNF-driven intestinal inflammation and dysbiosis by promoting innate immune responses of Paneth and dendritic cells.
Animals
Dendritic Cells
/ immunology
Dysbiosis
/ immunology
Humans
Immunity, Innate
/ immunology
Inflammation
/ immunology
Intestines
/ immunology
Mice
Mice, Knockout
Paneth Cells
/ immunology
Receptors, Tumor Necrosis Factor, Type I
/ deficiency
Receptors, Tumor Necrosis Factor, Type II
/ deficiency
Toll-Like Receptor 5
/ immunology
X-Linked Inhibitor of Apoptosis Protein
/ deficiency
Journal
Science immunology
ISSN: 2470-9468
Titre abrégé: Sci Immunol
Pays: United States
ID NLM: 101688624
Informations de publication
Date de publication:
05 Nov 2021
05 Nov 2021
Historique:
entrez:
5
11
2021
pubmed:
6
11
2021
medline:
8
3
2022
Statut:
ppublish
Résumé
Deficiency in X-linked inhibitor of apoptosis protein (XIAP) is the cause for X-linked lymphoproliferative syndrome 2 (XLP2). About one-third of these patients suffer from severe and therapy-refractory inflammatory bowel disease (IBD), but the exact cause of this pathogenesis remains undefined. Here, we used XIAP-deficient mice to characterize the mechanisms underlying intestinal inflammation. In
Identifiants
pubmed: 34739338
doi: 10.1126/sciimmunol.abf7235
doi:
Substances chimiques
Receptors, Tumor Necrosis Factor, Type I
0
Receptors, Tumor Necrosis Factor, Type II
0
TLR5 protein, human
0
TNFRSF1A protein, human
0
TNFRSF1B protein, human
0
Toll-Like Receptor 5
0
X-Linked Inhibitor of Apoptosis Protein
0
XIAP protein, human
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
eabf7235Subventions
Organisme : Austrian Science Fund FWF
ID : W 1226
Pays : Austria
Commentaires et corrections
Type : CommentIn