IL-33/Regulatory T-Cell Axis Suppresses Skin Fibrosis.
Alarmins
/ metabolism
Animals
Bleomycin
Cytokines
/ metabolism
Disease Models, Animal
Fibrosis
Forkhead Transcription Factors
/ metabolism
Humans
Interleukin-1 Receptor-Like 1 Protein
/ genetics
Interleukin-13
/ metabolism
Interleukin-33
/ metabolism
Mice
Scleroderma, Systemic
Skin
/ pathology
T-Lymphocytes, Regulatory
/ metabolism
Journal
The Journal of investigative dermatology
ISSN: 1523-1747
Titre abrégé: J Invest Dermatol
Pays: United States
ID NLM: 0426720
Informations de publication
Date de publication:
10 2022
10 2022
Historique:
received:
22
07
2021
revised:
08
02
2022
accepted:
03
03
2022
pubmed:
29
3
2022
medline:
28
9
2022
entrez:
28
3
2022
Statut:
ppublish
Résumé
Fibrosis is a pathological hallmark of systemic sclerosis, a deadly autoimmune disease affecting the connective tissues of multiple organs. However, the immune mechanisms underlying fibrosis and systemic sclerosis remain unclear. To determine the initiating immune pathway in fibrosis, we investigated the role of type 2 alarmin cytokines in the mouse model of skin fibrosis. Wild-type mice that received subcutaneous bleomycin injections developed skin fibrosis accompanied by elevated IL-33 expression in the dermis. Likewise, we found IL-33 upregulation in human skin fibrosis. Mice with germline deletion of IL-33 receptor (ST2 knockout) showed markedly exacerbated skin fibrosis in association with significantly increased T helper 2 cell to regulatory T-cell ratio in the skin. Mice that lacked ST2 specifically on regulatory T cells (Foxp3
Identifiants
pubmed: 35341735
pii: S0022-202X(22)00207-X
doi: 10.1016/j.jid.2022.03.009
pmc: PMC9511765
mid: NIHMS1792654
pii:
doi:
Substances chimiques
Alarmins
0
Cytokines
0
Forkhead Transcription Factors
0
Interleukin-1 Receptor-Like 1 Protein
0
Interleukin-13
0
Interleukin-33
0
Bleomycin
11056-06-7
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
2668-2676.e4Subventions
Organisme : NIAMS NIH HHS
ID : K08 AR068619
Pays : United States
Organisme : NIAMS NIH HHS
ID : R01 AR076013
Pays : United States
Informations de copyright
Copyright © 2022 The Authors. Published by Elsevier Inc. All rights reserved.
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