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Dysregulation of antiviral helicase pathways in systemic lupus erythematosus
In the autoimmune disease systemic lupus erythematosus (SLE), our normal antiviral defenses are inappropriately activated, resulting in over-activity of the type I interferon (IFN) pathway. This increased activity of the type I IFN pathway is an important primary pathogenic factor in the disease. Em...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4243696/ https://www.ncbi.nlm.nih.gov/pubmed/25505487 http://dx.doi.org/10.3389/fgene.2014.00418 |
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author | Oliveira, Luciana Sinicato, Nailú A. Postal, Mariana Appenzeller, Simone Niewold, Timothy B. |
author_facet | Oliveira, Luciana Sinicato, Nailú A. Postal, Mariana Appenzeller, Simone Niewold, Timothy B. |
author_sort | Oliveira, Luciana |
collection | PubMed |
description | In the autoimmune disease systemic lupus erythematosus (SLE), our normal antiviral defenses are inappropriately activated, resulting in over-activity of the type I interferon (IFN) pathway. This increased activity of the type I IFN pathway is an important primary pathogenic factor in the disease. Emerging evidence has implicated the antiviral helicases in this process. The antiviral helicases normally function as nucleic acid receptors in viral immunity. Genetic variations in antiviral helicase genes have been associated with SLE, supporting the idea that helicase pathways are involved in the primary pathogenesis of SLE. Studies have documented functional consequences of these genetic variations within the type I IFN pathway in human cell lines and SLE patients. In this review, we summarize the function of helicases in the anti-viral immune response, and how this response is dysregulated in SLE patients. In particular, we will focus on known functional genetic polymorphisms in the IFIH1 (MDA5) and mitochondrial antiviral signaling protein genes which have been implicated in human SLE. These data provide fascinating evidence for dysregulation of helicase-mediated innate immunity in SLE, and may support novel therapeutic strategies in the disease. |
format | Online Article Text |
id | pubmed-4243696 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-42436962014-12-10 Dysregulation of antiviral helicase pathways in systemic lupus erythematosus Oliveira, Luciana Sinicato, Nailú A. Postal, Mariana Appenzeller, Simone Niewold, Timothy B. Front Genet Genetics In the autoimmune disease systemic lupus erythematosus (SLE), our normal antiviral defenses are inappropriately activated, resulting in over-activity of the type I interferon (IFN) pathway. This increased activity of the type I IFN pathway is an important primary pathogenic factor in the disease. Emerging evidence has implicated the antiviral helicases in this process. The antiviral helicases normally function as nucleic acid receptors in viral immunity. Genetic variations in antiviral helicase genes have been associated with SLE, supporting the idea that helicase pathways are involved in the primary pathogenesis of SLE. Studies have documented functional consequences of these genetic variations within the type I IFN pathway in human cell lines and SLE patients. In this review, we summarize the function of helicases in the anti-viral immune response, and how this response is dysregulated in SLE patients. In particular, we will focus on known functional genetic polymorphisms in the IFIH1 (MDA5) and mitochondrial antiviral signaling protein genes which have been implicated in human SLE. These data provide fascinating evidence for dysregulation of helicase-mediated innate immunity in SLE, and may support novel therapeutic strategies in the disease. Frontiers Media S.A. 2014-11-25 /pmc/articles/PMC4243696/ /pubmed/25505487 http://dx.doi.org/10.3389/fgene.2014.00418 Text en Copyright © 2014 Oliveira, Sinicato, Postal, Appenzeller and Niewold. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Genetics Oliveira, Luciana Sinicato, Nailú A. Postal, Mariana Appenzeller, Simone Niewold, Timothy B. Dysregulation of antiviral helicase pathways in systemic lupus erythematosus |
title | Dysregulation of antiviral helicase pathways in systemic lupus erythematosus |
title_full | Dysregulation of antiviral helicase pathways in systemic lupus erythematosus |
title_fullStr | Dysregulation of antiviral helicase pathways in systemic lupus erythematosus |
title_full_unstemmed | Dysregulation of antiviral helicase pathways in systemic lupus erythematosus |
title_short | Dysregulation of antiviral helicase pathways in systemic lupus erythematosus |
title_sort | dysregulation of antiviral helicase pathways in systemic lupus erythematosus |
topic | Genetics |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4243696/ https://www.ncbi.nlm.nih.gov/pubmed/25505487 http://dx.doi.org/10.3389/fgene.2014.00418 |
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