Molecular biology of autoinflammatory diseases

作者：Junya Masumoto, Wei Zhou, Shinnosuke Morikawa, Sho Hosokawa, Haruka Taguchi, Toshihiro Yamamoto, Mie Kurata, Naoe Kaneko · 发表于：Inflammation and Regeneration · 年份：2021 · DOI：10.1186/s41232-021-00181-8 · 被引用次数：24 · 研究领域：Inflammasome and immune disorders、Gout, Hyperuricemia, Uric Acid、Atherosclerosis and Cardiovascular 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 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.