CHOP-mediated IL-23 overexpression does not drive colitis in experimental spondyloarthritis.
Animals
HLA-B27 Antigen
/ genetics
Transcription Factor CHOP
/ metabolism
Colitis
/ metabolism
Rats
Endoplasmic Reticulum Stress
Spondylarthritis
/ metabolism
Disease Models, Animal
Interleukin-23
/ metabolism
Humans
Interleukin-23 Subunit p19
/ genetics
Rats, Transgenic
Interleukin-17
/ metabolism
Colon
/ pathology
Macrophages
/ metabolism
Journal
Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288
Informations de publication
Date de publication:
29 05 2024
29 05 2024
Historique:
received:
06
12
2023
accepted:
22
05
2024
medline:
30
5
2024
pubmed:
30
5
2024
entrez:
29
5
2024
Statut:
epublish
Résumé
HLA-B27 is a major risk factor for spondyloarthritis (SpA), yet the underlying mechanisms remain unclear. HLA-B27 misfolding-induced IL-23, which is mediated by endoplasmic reticulum (ER) stress has been hypothesized to drive SpA pathogenesis. Expression of HLA-B27 and human β
Identifiants
pubmed: 38811719
doi: 10.1038/s41598-024-62940-0
pii: 10.1038/s41598-024-62940-0
doi:
Substances chimiques
HLA-B27 Antigen
0
Transcription Factor CHOP
147336-12-7
Interleukin-23
0
Ddit3 protein, rat
0
Interleukin-23 Subunit p19
0
Interleukin-17
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
12293Subventions
Organisme : NIAMS Intramural Research Program
ID : Z01 AR041184
Informations de copyright
© 2024. This is a U.S. Government work and not under copyright protection in the US; foreign copyright protection may apply.
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