Peripheral γδ T Cells Regulate Neutrophil Expansion and Recruitment in Experimental Psoriatic Arthritis.
Journal
Arthritis & rheumatology (Hoboken, N.J.)
ISSN: 2326-5205
Titre abrégé: Arthritis Rheumatol
Pays: United States
ID NLM: 101623795
Informations de publication
Date de publication:
09 2022
09 2022
Historique:
revised:
01
03
2022
received:
09
12
2021
accepted:
17
03
2022
pubmed:
24
3
2022
medline:
3
9
2022
entrez:
23
3
2022
Statut:
ppublish
Résumé
This study was undertaken to identify the mechanistic role of γδ T cells in the pathogenesis of experimental psoriatic arthritis (PsA). In this study, we performed interleukin-23 (IL-23) gene transfer in wild-type (WT) and T cell receptor δ-deficient (TCRδ We demonstrated that γδ T cells support systemic granulopoiesis, which is critical for murine PsA-like pathology. Briefly, γδ T cell ablation inhibited the expression of neutrophil chemokines CXCL1 and CXCL2 and neutrophil CD11b+Ly6G+ accumulation in the aforementioned PsA-related tissues. Although significantly reduced expression of granulocyte-macrophage colony-stimulating factor (GM-CSF) and IL-17A was detected systemically in TCRδ Our findings do not support the notion that tissue-resident γδ T cells initiate the disease but demonstrate a novel role of γδ T cells in neutrophil regulation that can be exploited therapeutically in PsA patients.
Identifiants
pubmed: 35320625
doi: 10.1002/art.42124
pmc: PMC9427669
mid: NIHMS1790960
doi:
Substances chimiques
Interleukin-17
0
Receptors, Antigen, T-Cell, gamma-delta
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1524-1534Subventions
Organisme : NIAMS NIH HHS
ID : R01 AR062173
Pays : United States
Informations de copyright
© 2022 American College of Rheumatology.
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