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Understanding IFNλ in rheumatoid arthritis

Unraveling the mechanisms underlying the inflammatory response in rheumatoid arthritis is crucial in order to better understand the disease and to develop novel therapeutic approaches. Although the effect of type I interferons on fibroblasts and in the context of rheumatoid arthritis has been descri...

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Detalles Bibliográficos
Autores principales: de Groen, Rik A, Liu, Bi-Sheng, Boonstra, André
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3978858/
https://www.ncbi.nlm.nih.gov/pubmed/24443794
http://dx.doi.org/10.1186/ar4445
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author de Groen, Rik A
Liu, Bi-Sheng
Boonstra, André
author_facet de Groen, Rik A
Liu, Bi-Sheng
Boonstra, André
author_sort de Groen, Rik A
collection PubMed
description Unraveling the mechanisms underlying the inflammatory response in rheumatoid arthritis is crucial in order to better understand the disease and to develop novel therapeutic approaches. Although the effect of type I interferons on fibroblasts and in the context of rheumatoid arthritis has been described for some time, little is known on the effects of the type III interferons, also known as IFNλ. In a previous issue, Xu and colleagues demonstrate that one of the members of the IFNλ family, IFNλ1, enhances Toll-like receptor expression and consequently promotes the production of proinflammatory cytokines known to be involved in initiating and maintaining the inflammatory responses in rheumatoid arthritis.
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spelling pubmed-39788582014-04-09 Understanding IFNλ in rheumatoid arthritis de Groen, Rik A Liu, Bi-Sheng Boonstra, André Arthritis Res Ther Editorial Unraveling the mechanisms underlying the inflammatory response in rheumatoid arthritis is crucial in order to better understand the disease and to develop novel therapeutic approaches. Although the effect of type I interferons on fibroblasts and in the context of rheumatoid arthritis has been described for some time, little is known on the effects of the type III interferons, also known as IFNλ. In a previous issue, Xu and colleagues demonstrate that one of the members of the IFNλ family, IFNλ1, enhances Toll-like receptor expression and consequently promotes the production of proinflammatory cytokines known to be involved in initiating and maintaining the inflammatory responses in rheumatoid arthritis. BioMed Central 2014 2014-01-21 /pmc/articles/PMC3978858/ /pubmed/24443794 http://dx.doi.org/10.1186/ar4445 Text en Copyright © 2014 BioMed Central Ltd.
spellingShingle Editorial
de Groen, Rik A
Liu, Bi-Sheng
Boonstra, André
Understanding IFNλ in rheumatoid arthritis
title Understanding IFNλ in rheumatoid arthritis
title_full Understanding IFNλ in rheumatoid arthritis
title_fullStr Understanding IFNλ in rheumatoid arthritis
title_full_unstemmed Understanding IFNλ in rheumatoid arthritis
title_short Understanding IFNλ in rheumatoid arthritis
title_sort understanding ifnλ in rheumatoid arthritis
topic Editorial
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3978858/
https://www.ncbi.nlm.nih.gov/pubmed/24443794
http://dx.doi.org/10.1186/ar4445
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