Autoinflammatory diseases: what is behind them and what is new?
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Page Press Publications
Abstract
Autoinflammatory diseases are characterized by bouts of systemic or localized inflammation in the absence of an infection. While some autoinflammatory diseases are caused by a single gene mutation, others have been shown to be multifactorial, involving a large array of genes coupled with environmental factors. Previous studies briefly elucidated the molecular mechanisms behind the many autoinflammatory diseases, focusing on the dysregulation of interleukin (IL)-1β or IL-18, nuclear factor-κB activation, and Interferons secretion. In this review, we precisely highlight the autoinflammatory disease-specific signalosomes, and we aim to provide a scaffold of the link between the various affected pathways. ©Copyright: the Author(s), 2023.
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Autoinflammatory diseases, Molecular dysregulation, Signalosomes, 1,2,3,6 tetrahydro 1 methyl 4 phenylpyridine, Coatomer protein, Cyclic gmp, Cytokine, Inflammasome, Interferon, Interleukin 1, Interleukin 1 receptor, Interleukin 18, Interleukin 1beta, Mevalonate kinase, Mitochondrial permeability transition pore, Proteasome, Reactive oxygen metabolite, Tumor necrosis factor receptor, Voltage dependent anion channel, Acne, Arthritis, Article, Autoinflammatory disease, Blau syndrome, Calcium transport, Cell damage, Cell vacuole, Cryopyrin-associated periodic syndrome, Dyskeratosis, Endoplasmic reticulum, Familial mediterranean fever, Gene mutation, Gene product, Haploinsufficiency, Human, Inflammation, Interferonopathy, Lipodystrophy, Mevalonate kinase deficiency, Mutation, Nf kb signaling, Papa syndrome, Pathophysiology, Pyoderma gangrenosum, Pyrin domain, Sarcoidosis, Skin disease, Temperature, Tissue injury, Tumor necrosis factor receptor associated periodic syndrome