Transferrin receptor 2 deficiency promotes macrophage polarization and inflammatory arthritis.
Journal
Redox biology
ISSN: 2213-2317
Titre abrégé: Redox Biol
Pays: Netherlands
ID NLM: 101605639
Informations de publication
Date de publication:
04 2023
04 2023
Historique:
received:
23
12
2022
revised:
19
01
2023
accepted:
24
01
2023
pubmed:
7
2
2023
medline:
22
2
2023
entrez:
6
2
2023
Statut:
ppublish
Résumé
Rheumatoid arthritis is an inflammatory joint disease in which synovial iron deposition has been described. Transferrin receptor 2 (Tfr2) represents a critical regulator of systemic iron levels. Loss of Tfr2 function in humans and mice results in iron overload. As iron contributes to inflammatory processes, we investigated whether Tfr2-deletion affects the pathogenesis of inflammatory arthritis in an iron-dependent manner. Using a global and conditional genetic disruption of Tfr2, we assessed the relevance of Tfr2 in K/BxN serum-transfer arthritis (STA) and macrophage polarization. Male Tfr2 Taken together, these findings suggest a protective role of Tfr2 in macrophages on the progression of arthritis via suppression of M1-like polarization.
Identifiants
pubmed: 36746004
pii: S2213-2317(23)00017-4
doi: 10.1016/j.redox.2023.102616
pmc: PMC9932570
pii:
doi:
Substances chimiques
Iron
E1UOL152H7
Receptors, Transferrin
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
102616Informations de copyright
Copyright © 2023 The Authors. Published by Elsevier B.V. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of competing interest LCH received support for clinical trials to his institution from Alexion, Ascendis, Takeda, and UCB. MR received honoraria for lectures from UCB. All other authors have no financial conflicts of interest.
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