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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...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2014
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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. |
format | Online Article Text |
id | pubmed-3978858 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
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 |
work_keys_str_mv | AT degroenrika understandingifnlinrheumatoidarthritis AT liubisheng understandingifnlinrheumatoidarthritis AT boonstraandre understandingifnlinrheumatoidarthritis |