| Campo DC | Valor | Idioma |
|---|
| dc.contributor.author | Pinto, Larissa G. | - |
| dc.contributor.author | Talbot, Jhimmy | - |
| dc.contributor.author | Peres, Raphael S. | - |
| dc.contributor.author | Franca, Rafael F. | - |
| dc.contributor.author | Ferreira, Sérgio Henrique | - |
| dc.contributor.author | Ryffel, Bernhard | - |
| dc.contributor.author | Alves-Filho, José Carlos F. | - |
| dc.contributor.author | Cavalcanti Neto, Florêncio Figueiredo | - |
| dc.contributor.author | Cunha, Thiago Mattar | - |
| dc.contributor.author | Cunha, Fernando de Queiroz | - |
| dc.date.accessioned | 2021-08-14T14:27:37Z | - |
| dc.date.available | 2021-08-14T14:27:37Z | - |
| dc.date.issued | 2015 | - |
| dc.identifier.citation | PINTO, Larissa G. et al. Joint production of IL-22 participates in the initial phase of antigen-induced arthritis through IL-1β production. Arthritis Research & Therapy , v. 17, 235, 2015. DOI: https://doi.org/10.1186/s13075-015-0759-2. Disponível em: https://arthritis-research.biomedcentral.com/articles/10.1186/s13075-015-0759-2. Acesso em: 17 maio 2021. | pt_BR |
| dc.identifier.uri | https://repositorio.unb.br/handle/10482/41716 | - |
| dc.language.iso | Inglês | pt_BR |
| dc.publisher | BioMed Central | pt_BR |
| dc.rights | Acesso Aberto | pt_BR |
| dc.title | Joint production of IL-22 participates in the initial phase of antigen-induced arthritis through IL-1β production | pt_BR |
| dc.type | Artigo | pt_BR |
| dc.subject.keyword | Ratos | pt_BR |
| dc.subject.keyword | Imunização | pt_BR |
| dc.subject.keyword | Neutrófilos | pt_BR |
| dc.subject.keyword | Artrite reumatoide | pt_BR |
| dc.rights.license | (CC BY) - © 2015 Pinto et al. Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. | pt_BR |
| dc.identifier.doi | https://doi.org/10.1186/s13075-015-0759-2 | pt_BR |
| dc.description.abstract1 | Introduction: Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by neutrophil articular
infiltration, joint pain and the progressive destruction of cartilage and bone. IL-22 is a key effector molecule that
plays a critical role in autoimmune diseases. However, the function of IL-22 in the pathogenesis of RA remains
controversial. In this study, we investigated the role of IL-22 in the early phase of antigen-induced arthritis (AIA) in mice.
Methods: AIA was induced in C57BL/6, IL-22−/−
, ASC−/− and IL-1R1−/− immunized mice challenged intra-articularly with
methylated bovine serum albumin (mBSA). Expression of IL-22 in synovial membranes was determined by RT-PCR.
Articular hypernociception was evaluated using an electronic von Frey. Neutrophil recruitment and histopathological
analyses were assessed in inflamed knee joint. Joint levels of inflammatory mediators and mBSA-specific IgG
concentration in the serum were measured by ELISA.
Results: The IL-22 mRNA expression and protein levels in synovial tissue were increased during the onset of AIA.
In addition, pharmacological inhibition (anti-IL-22 antibody) and genetic deficiency (IL-22−/− mice) reduced
articular pain and neutrophil migration in arthritic mice. Consistent with these findings, recombinant IL-22 joint
administration promoted articular inflammation per se in WT mice, restoring joint nociception and neutrophil
infiltration in IL-22−/− mice. Moreover, IL-22-deficient mice showed reduced synovitis (inflammatory cell influx)
and lower joint IL-1β levels, whereas the production of IL-17, MCP-1/CCL2, and KC/CXCL1 and the humoral
immune response were similar, compared with WT mice. Corroborating these results, the exogenous administration of
IL-22 into the joints induced IL-1β production in WT mice and reestablished IL-1β production in IL-22−/− mice
challenged with mBSA. Additionally, IL-1R1−/− mice showed attenuated inflammatory features induced by mBSA
or IL-22 challenge. Articular nociception and neutrophil migration induced by IL-22 were also reduced in ASC−/− mice.
Conclusions: These results suggest that IL-22 plays a pro-inflammatory/pathogenic role in the onset of AIA through an
ASC-dependent stimulation of IL-1β production. | pt_BR |
| dc.description.unidade | Faculdade de Medicina (FMD) | - |
| Aparece nas coleções: | Artigos publicados em periódicos e afins
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