Molecular biology of autoinflammatory diseases
Abstract 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-asso...
| Main Authors: | , , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
BMC
2021-10-01
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| Series: | Inflammation and Regeneration |
| Subjects: | |
| Online Access: | https://doi.org/10.1186/s41232-021-00181-8 |
| _version_ | 1818724713784934400 |
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| author | Junya Masumoto Wei Zhou Shinnosuke Morikawa Sho Hosokawa Haruka Taguchi Toshihiro Yamamoto Mie Kurata Naoe Kaneko |
| author_facet | Junya Masumoto Wei Zhou Shinnosuke Morikawa Sho Hosokawa Haruka Taguchi Toshihiro Yamamoto Mie Kurata Naoe Kaneko |
| author_sort | Junya Masumoto |
| collection | DOAJ |
| description | Abstract 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. |
| first_indexed | 2024-12-17T21:30:48Z |
| format | Article |
| id | doaj.art-70d7aff5e3b0451ab4273d60ce5b8351 |
| institution | Directory Open Access Journal |
| issn | 1880-8190 |
| language | English |
| last_indexed | 2024-12-17T21:30:48Z |
| publishDate | 2021-10-01 |
| publisher | BMC |
| record_format | Article |
| series | Inflammation and Regeneration |
| spelling | doaj.art-70d7aff5e3b0451ab4273d60ce5b83512022-12-21T21:31:53ZengBMCInflammation and Regeneration1880-81902021-10-0141112610.1186/s41232-021-00181-8Molecular biology of autoinflammatory diseasesJunya Masumoto0Wei Zhou1Shinnosuke Morikawa2Sho Hosokawa3Haruka Taguchi4Toshihiro Yamamoto5Mie Kurata6Naoe Kaneko7Department of Pathology, Ehime University Graduate School of Medicine and Proteo-Science CenterDepartment of Pathology, Ehime University Graduate School of Medicine and Proteo-Science CenterDepartment of Pathology, Ehime University Graduate School of Medicine and Proteo-Science CenterDepartment of Pathology, Ehime University Graduate School of Medicine and Proteo-Science CenterDepartment of Pathology, Ehime University Graduate School of Medicine and Proteo-Science CenterDepartment of Pathology, Ehime University Graduate School of Medicine and Proteo-Science CenterDepartment of Pathology, Ehime University Graduate School of Medicine and Proteo-Science CenterDepartment of Pathology, Ehime University Graduate School of Medicine and Proteo-Science CenterAbstract 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.https://doi.org/10.1186/s41232-021-00181-8Interleukin-1NF-κBType I interferonAutoinflammatory diseases |
| spellingShingle | Junya Masumoto Wei Zhou Shinnosuke Morikawa Sho Hosokawa Haruka Taguchi Toshihiro Yamamoto Mie Kurata Naoe Kaneko Molecular biology of autoinflammatory diseases Inflammation and Regeneration Interleukin-1 NF-κB Type I interferon 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 | Interleukin-1 NF-κB Type I interferon Autoinflammatory diseases |
| url | https://doi.org/10.1186/s41232-021-00181-8 |
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