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.
Highlights
The human body has evolved various adaptive responses that protect against cell and tissue damage caused by physical, chemical, and biological factors
Such factors include molecules released by damaged tissues, metabolites, and/or infection [1–4]
Inflammation, an adaptive response to cell injury, generates damage-associated molecular patterns (DAMPs) and/or pathogen-associated molecular patterns (PAMPs), which are recognized by pattern recognition receptors (PRRs) expressed mainly by innate immune cells [5]
Summary
The human body has evolved various adaptive responses that protect against cell and tissue damage caused by physical, chemical, and biological factors. RNase activity against viral RNA Infections and aberrant inflammatory responses: SLE and other autoimmune diseases [75, 76]
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