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http://hdl.handle.net/2445/120023
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DC Field | Value | Language |
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dc.contributor.author | Ripoll Llagostera, Èlia | - |
dc.contributor.author | Ramon, Laura de | - |
dc.contributor.author | Bordignon Draibe, Juliana | - |
dc.contributor.author | Merino, Ana | - |
dc.contributor.author | Bolaños, Núria | - |
dc.contributor.author | Gomà, Montse | - |
dc.contributor.author | Cruzado, Josep Ma. | - |
dc.contributor.author | Grinyó Boira, Josep M. | - |
dc.contributor.author | Torras Ambròs, Joan | - |
dc.date.accessioned | 2018-02-20T09:46:03Z | - |
dc.date.available | 2018-02-20T09:46:03Z | - |
dc.date.issued | 2016-06-08 | - |
dc.identifier.issn | 1478-6362 | - |
dc.identifier.uri | http://hdl.handle.net/2445/120023 | - |
dc.description | Es va publicar un erratum de l'article a: Arthritis Research & Therapy, 2016, vol. 18 , num. 1, p. 152 | - |
dc.description.abstract | Background: Lupus nephritis (LN) is a complex chronic autoimmune disease of unknown etiology characterized by loss of tolerance against several self-antigens. Cytokines are known to be central players in LN pathogenesis. The Janus kinase-signal transducer and activator of transcription (JAK-STAT) pathway is one important pathway that mediates signal transduction of several cytokines. In this study, we examined the pathogenic role of this pathway and how CP-690,550 treatment influences LN outcome. Methods: Six-month-old NZB/NZWF1 mice were divided into two different treatment groups: (1) control animals given vehicle treatment, cyclophosphamide, and mycophenolate mofetil treatment as positive controls of the therapy and (2) mice treated with CP-690,550, a JAK3 inhibitor. Mice were treated for 12 weeks. We evaluated renal function, anti-double-stranded DNA (anti-dsDNA) antibody, renal histology changes, kidney complement and immunoglobulin G (IgG) deposits, T-cell and macrophage infiltration, kidney inflammatory gene expression, and circulating cytokine changes. Results: CP-690,550 treatment significantly reduced proteinuria and improved renal function and histological lesions of the kidney. Compared with vehicle-treated animals, those undergoing CP-690,550 treatment showed significantly diminished anti-dsDNA antibody and complement component C3 and IgG deposition in glomeruli. We also observed a significant reduction of T-cell and macrophage infiltration. Kidney gene expression revealed a reduction in inflammatory cytokines and complement and related macrophage-attracting genes. Circulating inflammatory cytokines were also reduced with treatment. Conclusions: On the basis of our results, we conclude that the JAK-STAT pathway is implicated in the progression of renal inflammation in NZB/WF1 mice and that targeting JAK3 with CP-690,550 is effective in slowing down the course of experimental LN. Thus, CP-690,550 could become a new therapeutic tool in LN and other autoimmune diseases. | - |
dc.format.extent | 12 p. | - |
dc.format.mimetype | application/pdf | - |
dc.language.iso | eng | - |
dc.publisher | BioMed Central | - |
dc.relation.isformatof | Reproducció del document publicat a: https://doi.org/10.1186/s13075-016-1034-x | - |
dc.relation.ispartof | Arthritis Research & Therapy, 2016, vol. 18 , num. 1, p. 134 | - |
dc.relation.uri | https://doi.org/10.1186/s13075-016-1034-x | - |
dc.rights | cc-by (c) Ripoll Llagostera, Èlia et al., 2016 | - |
dc.rights.uri | http://creativecommons.org/licenses/by/3.0/es | - |
dc.source | Articles publicats en revistes (Ciències Clíniques) | - |
dc.subject.classification | Lupus | - |
dc.subject.classification | Malalties autoimmunitàries | - |
dc.subject.classification | Citoquines | - |
dc.subject.classification | Ratolins (Animals de laboratori) | - |
dc.subject.other | Lupus | - |
dc.subject.other | Autoimmune diseases | - |
dc.subject.other | Cytokines | - |
dc.subject.other | Mice (Laboratory animals) | - |
dc.title | JAK3-STAT pathway blocking benefits in experimental lupus nephritis | - |
dc.type | info:eu-repo/semantics/article | - |
dc.type | info:eu-repo/semantics/publishedVersion | - |
dc.identifier.idgrec | 666380 | - |
dc.date.updated | 2018-02-20T09:46:03Z | - |
dc.rights.accessRights | info:eu-repo/semantics/openAccess | - |
dc.identifier.pmid | 27278657 | - |
Appears in Collections: | Articles publicats en revistes (Institut d'lnvestigació Biomèdica de Bellvitge (IDIBELL)) Articles publicats en revistes (Ciències Clíniques) |
Files in This Item:
File | Description | Size | Format | |
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666380.pdf | 2.2 MB | Adobe PDF | View/Open | |
666380 Erratum.pdf | 333.91 kB | Adobe PDF | View/Open |
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