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Inhibition of the TWEAK/Fn14 pathway attenuates autoimmune arthritis in a SKG mouse model

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dc.contributor.authorPark, Jin Sil
dc.contributor.authorKim, Sung Min
dc.contributor.authorJung, Kyung Ah
dc.contributor.authorLee, Jennifer
dc.contributor.authorKwok, Seung Ki
dc.contributor.authorCho, Mi La
dc.contributor.authorPark, Sung Hwan
dc.date.accessioned2022-02-21T10:07:06Z
dc.date.available2022-02-21T10:07:06Z
dc.date.issued2017
dc.description.abstractTumor necrosis factor-like weak inducer of apoptosis (TWEAK) is a proinflammatory cytokine that is involved in pathogenesis of abnormal or disregulated inflammation. To verify how TWEAK/fibroblast growth factor-inducible gene 14 (Fn14) signals affect development of Th17 cells in arthritis, we utilized the SKG mouse, which spontaneously develops Th17- mediated autoimmune arthritis. Fn14-Fc was administered to zymosan A-induced arthritogenic SKG mice, and the effects in vivo were examined. Destruction of cartilage and bone damage was assessed by Hematoxylin and Eosin, and safranin O staining of the affected tissues. Phenotypic analysis of cells expressing inflammatory cytokines and angiogenesis-related factors, and the expression of transcription factor STAT3 in the affected joints were determined by immunohistochemistry. Blockade of Fn14 with Fn14-Fc reduced the clinical and histologic scores of inflammatory arthritis in the mouse model of spontaneously developed chronic autoimmune arthritis. Fn14-Fc suppressed production of inflammatory cytokines and angiogenesis-promoting factors, such as vascular endothelial growth factor and matrix metalloproteinase 3. Moreover, blocking of the TWEAK signal inhibited expression of STAT3 as well as interleukin-17 and -21 produced by Th17 cells. These results implicate TWEAK as a potential molecular target for treatment or prevention of inflammatory arthritis and autoimmune diseases such as rheumatoid arthritis.es
dc.formatapplication/pdfes
dc.format.extent10es
dc.identifier.citationHistology and Histopathology, Vol.32, nÂş5, (2017)
dc.identifier.doiDOI: 10.14670/HH-11-813
dc.identifier.issn1699-5848
dc.identifier.issn0213-3911
dc.identifier.urihttp://hdl.handle.net/10201/117203
dc.languageenges
dc.publisherUniversidad de Murcia. Departamento de BiologĂ­a Celular e HistologĂ­aes
dc.relationSin financiaciĂłn externa a la Universidades
dc.rightsinfo:eu-repo/semantics/openAccesses
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectTWEAKes
dc.subjectSKG micees
dc.subjectSTAT3es
dc.subjectIL-17- producing T cellses
dc.subjectAngiogenesises
dc.subject.otherCDU::6 - Ciencias aplicadas::61 - Medicina::616 - PatologĂ­a. Medicina clĂ­nica. OncologĂ­aes
dc.titleInhibition of the TWEAK/Fn14 pathway attenuates autoimmune arthritis in a SKG mouse modeles
dc.typeinfo:eu-repo/semantics/articlees
dspace.entity.typePublicationes
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Histology and histopathology Vol.32, nÂş5 (2017)