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Molecular biology of autoinflammatory diseases.

Junya MasumotoWei ZhouShinnosuke MorikawaSho HosokawaHaruka TaguchiToshihiro YamamotoMie KurataNaoe Kaneko
Published in: Inflammation and regeneration (2021)
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.
Keyphrases
  • oxidative stress
  • immune response
  • signaling pathway
  • induced apoptosis
  • physical activity
  • dendritic cells
  • ms ms
  • bone marrow
  • single cell
  • cell cycle arrest
  • lps induced
  • cell proliferation
  • inflammatory response