DAMP-mediated inflammation and regulated cell death in immunoinflammatory rheumatic diseases

The state of autoreactivity innate immunity dominates in the pathogenesis immunoinflammatory rheumatic diseases, inducing non-infectious “sterile” inflammation. distinctive properties this inflammation include multiorgan affection and recurrent clinical course. extracellular intracellular “danger signals” called DAMPs, seem to be a key factor progression inflammatory events. These factors are released by loose fibrous connective tissue course main substance disorganization, as well regulated accidental local cell death. In immune/inflammatory DAMP-induced patterns death autophagy, apoptosis, necroptosis, pyroptosis netosis. Membrane cytosolic PRR receptors, interacting with promote these forms At same time, modes often combined simultaneous reaction receptors pathogens that preexist dead cells. TLR-DAMP interaction activates similar signaling pathways, adaptive molecules, transcription factors, forming pro-inflammatory inflammasomes TLR-PAMP interaction. processes, antigen-presenting function dendritic cells is expressed maximal extent. Given important role infections etiological processes may phenomenon antigenic cross-presentation. Interactions DAMPs cause formation DAMP-mediated vicious circle. increased levels proinflammatory both situ systemic circulation, leads, via PRR-DAMP interactions, incresing number prone even more pronounced damage. turn, significantly increase tissues, thus causing diseases. have been identified all types induced available research results allow us determine appropriate targets which subjected pharmacological correction. respect, significant progress has made search for medicinal tools regulating SLE, RA, Sjogren’s syndrome, SSD, etc. Of sufficient importance evaluation serum DAMP diagnostic prognostic biomarkers, along their determination assessing treatment efficiency