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Dysregulated IL-1β Secretion in Autoinflammatory Diseases: A Matter of Stress?
Infectious and sterile inflammation is induced by activation of innate immune cells. Triggering of toll-like receptors by pathogen-associated molecular pattern or damage-associated molecular pattern (PAMP or DAMP) molecules generates reactive oxygen species that in turn induce production and activat...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5378711/ https://www.ncbi.nlm.nih.gov/pubmed/28421072 http://dx.doi.org/10.3389/fimmu.2017.00345 |
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author | Carta, Sonia Semino, Claudia Sitia, Roberto Rubartelli, Anna |
author_facet | Carta, Sonia Semino, Claudia Sitia, Roberto Rubartelli, Anna |
author_sort | Carta, Sonia |
collection | PubMed |
description | Infectious and sterile inflammation is induced by activation of innate immune cells. Triggering of toll-like receptors by pathogen-associated molecular pattern or damage-associated molecular pattern (PAMP or DAMP) molecules generates reactive oxygen species that in turn induce production and activation of pro-inflammatory cytokines such as IL-1β. Recent evidence indicates that cell stress due to common events, like starvation, enhanced metabolic demand, cold or heat, not only potentiates inflammation but may also directly trigger it in the absence of PAMPs or DAMPs. Stress-mediated inflammation is also a common feature of many hereditary disorders, due to the proteotoxic effects of mutant proteins. We propose that harmful mutant proteins can induce dysregulated IL-1β production and inflammation through different pathways depending on the cell type involved. When expressed in professional inflammatory cells, stress induced by the mutant protein activates in a cell-autonomous way the onset of inflammation and mediates its aberrant development, resulting in the explosive responses that hallmark autoinflammatory diseases. When expressed in non-immune cells, the mutant protein may cause the release of transcellular stress signals that trigger and propagate inflammation. |
format | Online Article Text |
id | pubmed-5378711 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-53787112017-04-18 Dysregulated IL-1β Secretion in Autoinflammatory Diseases: A Matter of Stress? Carta, Sonia Semino, Claudia Sitia, Roberto Rubartelli, Anna Front Immunol Immunology Infectious and sterile inflammation is induced by activation of innate immune cells. Triggering of toll-like receptors by pathogen-associated molecular pattern or damage-associated molecular pattern (PAMP or DAMP) molecules generates reactive oxygen species that in turn induce production and activation of pro-inflammatory cytokines such as IL-1β. Recent evidence indicates that cell stress due to common events, like starvation, enhanced metabolic demand, cold or heat, not only potentiates inflammation but may also directly trigger it in the absence of PAMPs or DAMPs. Stress-mediated inflammation is also a common feature of many hereditary disorders, due to the proteotoxic effects of mutant proteins. We propose that harmful mutant proteins can induce dysregulated IL-1β production and inflammation through different pathways depending on the cell type involved. When expressed in professional inflammatory cells, stress induced by the mutant protein activates in a cell-autonomous way the onset of inflammation and mediates its aberrant development, resulting in the explosive responses that hallmark autoinflammatory diseases. When expressed in non-immune cells, the mutant protein may cause the release of transcellular stress signals that trigger and propagate inflammation. Frontiers Media S.A. 2017-04-04 /pmc/articles/PMC5378711/ /pubmed/28421072 http://dx.doi.org/10.3389/fimmu.2017.00345 Text en Copyright © 2017 Carta, Semino, Sitia and Rubartelli. 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 | Immunology Carta, Sonia Semino, Claudia Sitia, Roberto Rubartelli, Anna Dysregulated IL-1β Secretion in Autoinflammatory Diseases: A Matter of Stress? |
title | Dysregulated IL-1β Secretion in Autoinflammatory Diseases: A Matter of Stress? |
title_full | Dysregulated IL-1β Secretion in Autoinflammatory Diseases: A Matter of Stress? |
title_fullStr | Dysregulated IL-1β Secretion in Autoinflammatory Diseases: A Matter of Stress? |
title_full_unstemmed | Dysregulated IL-1β Secretion in Autoinflammatory Diseases: A Matter of Stress? |
title_short | Dysregulated IL-1β Secretion in Autoinflammatory Diseases: A Matter of Stress? |
title_sort | dysregulated il-1β secretion in autoinflammatory diseases: a matter of stress? |
topic | Immunology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5378711/ https://www.ncbi.nlm.nih.gov/pubmed/28421072 http://dx.doi.org/10.3389/fimmu.2017.00345 |
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