Molecular biology of autoinflammatory diseases
Summary
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. © 2021. The Author(s).
| Authors | Masumoto J, Zhou W, Morikawa S, Hosokawa S, Taguchi H, Yamamoto T, Kurata M, Kaneko N |
|---|---|
| Journal | Inflammation and regeneration |
| Publication Date | 2021 Oct 11;41(1):33 |
| PubMed | 34635190 |
| PubMed Central | PMC8507398 |
| DOI | 10.1186/s41232-021-00181-8 |