IL-22 increases the production of sFRP3 by FLS in inflammatory joint diseases

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MetadadosDescriçãoIdioma
Autor(es): dc.creatorResende, G. G.-
Autor(es): dc.creatorMachado, C. R. L.-
Autor(es): dc.creatorRocha, M. A.-
Autor(es): dc.creatorMacedo, R. B. V.-
Autor(es): dc.creatorBueno Filho, J. S. S.-
Autor(es): dc.creatorKakehasi, A. M.-
Autor(es): dc.creatorAndrade, M. V.-
Data de aceite: dc.date.accessioned2026-02-09T12:06:27Z-
Data de disponibilização: dc.date.available2026-02-09T12:06:27Z-
Data de envio: dc.date.issued2021-09-14-
Data de envio: dc.date.issued2021-09-14-
Data de envio: dc.date.issued2020-08-
Fonte completa do material: dc.identifierhttps://repositorio.ufla.br/handle/1/48128-
Fonte: dc.identifier.urihttp://educapes.capes.gov.br/handle/capes/1154448-
Descrição: dc.descriptionRheumatoid arthritis (RA), psoriatic arthritis (PsA), and ankylosing spondylitis (AS) are inflammatory diseases with different bone remodeling patterns. Fibroblast-like synoviocytes (FLS) are cells involved in the transition from an acute and reparable phase to a chronic and persistent stage in these diseases. The distinction of joint phenotypes involves inflammatory cytokines such as tumor necrosis factor alpha (TNF-α), interleukin (IL)-17, and IL-22 directly or through key signaling pathways such as Wnt. To evaluate the role of FLS as the source of Wnt antagonists (sFRP3/FRZB and Dkk1) in the synovia, levels of TNF- α, IL-17, IL-22, Dkk1, and sFRP3 were measured by ELISA directly in the synovial fluid of patients with RA, PsA, or AS. Dkk1 and sFRP3 were also measured in the FLS culture supernatants after different inflammatory stimulus. sFRP3 and Dkk1 are constitutively expressed by FLS. IL-22 and sFRP3 were positively correlated (r=0.76; P<0.01) in synovial fluid. The stimulation of FLS with IL-22, but not TNF-alpha and IL-17, increased the production of sFRP3. No stimulus altered the basal expression of Dkk1. These results showed, for the first time, the ability of IL-22 to increase the expression of sFRP3/FRZB by human FLS in both in vitro and ex vivo models. This finding linked IL-22 to local inhibition of Wnt signaling and possibly to blockade of osteogenesis. Furthermore, FLS presented as a source of this inhibitor in synovial fluid, assigning to this cell a bone injury mechanism.-
Formato: dc.formatapplication/pdf-
Idioma: dc.languageen-
Publicador: dc.publisherAssociação Brasileira de Divulgação Científica-
Direitos: dc.rightsacesso aberto-
Direitos: dc.rightshttp://creativecommons.org/licenses/by/4.0/-
Direitos: dc.rightshttp://creativecommons.org/licenses/by/4.0/-
???dc.source???: dc.sourceBrazilian Journal of Medical and Biological Research-
Palavras-chave: dc.subjectWnt signaling pathway-
Palavras-chave: dc.subjectFibroblast-like synoviocytes-
Palavras-chave: dc.subjectRheumatoid arthritis-
Palavras-chave: dc.subjectSpondyloarthritis-
Palavras-chave: dc.subjectVia de sinalização da Wnt-
Palavras-chave: dc.subjectSinoviócitos semelhantes a fibroblastos-
Palavras-chave: dc.subjectArtrite reumatóide-
Palavras-chave: dc.subjectEspondiloartrites-
Palavras-chave: dc.subjectDoenças inflamatórias-
Título: dc.titleIL-22 increases the production of sFRP3 by FLS in inflammatory joint diseases-
Tipo de arquivo: dc.typeArtigo-
Aparece nas coleções:Repositório Institucional da Universidade Federal de Lavras (RIUFLA)

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