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Molecular biology of autoinflammatory diseases
The long battle between humans and various physical, chemical, and biological insults that cause cell injury (e.g., products of tissue damage, metabolites, and/or infections) have led to the evolution of various adaptive responses. These responses are triggered by recognition of damage-associated mo...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8507398/ https://www.ncbi.nlm.nih.gov/pubmed/34635190 http://dx.doi.org/10.1186/s41232-021-00181-8 |
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author | Masumoto, Junya Zhou, Wei Morikawa, Shinnosuke Hosokawa, Sho Taguchi, Haruka Yamamoto, Toshihiro Kurata, Mie Kaneko, Naoe |
author_facet | Masumoto, Junya Zhou, Wei Morikawa, Shinnosuke Hosokawa, Sho Taguchi, Haruka Yamamoto, Toshihiro Kurata, Mie Kaneko, Naoe |
author_sort | Masumoto, Junya |
collection | PubMed |
description | The long battle between humans and various physical, chemical, and biological insults that cause cell injury (e.g., products of tissue damage, metabolites, and/or infections) have led to the evolution of various adaptive responses. These responses are triggered by recognition of damage-associated molecular patterns (DAMPs) and/or pathogen-associated molecular patterns (PAMPs), usually by cells of the innate immune system. DAMPs and PAMPs are recognized by pattern recognition receptors (PRRs) expressed by innate immune cells; this recognition triggers inflammation. Autoinflammatory diseases are strongly associated with dysregulation of PRR interactomes, which include inflammasomes, NF-κB-activating signalosomes, type I interferon-inducing signalosomes, and immuno-proteasome; disruptions of regulation of these interactomes leads to inflammasomopathies, relopathies, interferonopathies, and proteasome-associated autoinflammatory syndromes, respectively. In this review, we discuss the currently accepted molecular mechanisms underlying several autoinflammatory diseases. |
format | Online Article Text |
id | pubmed-8507398 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-85073982021-10-20 Molecular biology of autoinflammatory diseases Masumoto, Junya Zhou, Wei Morikawa, Shinnosuke Hosokawa, Sho Taguchi, Haruka Yamamoto, Toshihiro Kurata, Mie Kaneko, Naoe Inflamm Regen Review The long battle between humans and various physical, chemical, and biological insults that cause cell injury (e.g., products of tissue damage, metabolites, and/or infections) have led to the evolution of various adaptive responses. These responses are triggered by recognition of damage-associated molecular patterns (DAMPs) and/or pathogen-associated molecular patterns (PAMPs), usually by cells of the innate immune system. DAMPs and PAMPs are recognized by pattern recognition receptors (PRRs) expressed by innate immune cells; this recognition triggers inflammation. Autoinflammatory diseases are strongly associated with dysregulation of PRR interactomes, which include inflammasomes, NF-κB-activating signalosomes, type I interferon-inducing signalosomes, and immuno-proteasome; disruptions of regulation of these interactomes leads to inflammasomopathies, relopathies, interferonopathies, and proteasome-associated autoinflammatory syndromes, respectively. In this review, we discuss the currently accepted molecular mechanisms underlying several autoinflammatory diseases. BioMed Central 2021-10-11 /pmc/articles/PMC8507398/ /pubmed/34635190 http://dx.doi.org/10.1186/s41232-021-00181-8 Text en © The Author(s) 2021 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Review Masumoto, Junya Zhou, Wei Morikawa, Shinnosuke Hosokawa, Sho Taguchi, Haruka Yamamoto, Toshihiro Kurata, Mie Kaneko, Naoe Molecular biology of autoinflammatory diseases |
title | Molecular biology of autoinflammatory diseases |
title_full | Molecular biology of autoinflammatory diseases |
title_fullStr | Molecular biology of autoinflammatory diseases |
title_full_unstemmed | Molecular biology of autoinflammatory diseases |
title_short | Molecular biology of autoinflammatory diseases |
title_sort | molecular biology of autoinflammatory diseases |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8507398/ https://www.ncbi.nlm.nih.gov/pubmed/34635190 http://dx.doi.org/10.1186/s41232-021-00181-8 |
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