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. 2021 Feb 5;10(4):605. doi: 10.3390/jcm10040605

Figure 1.

Figure 1

Schematic overview of the pathogenesis for IL-1-mediated autoimmune disease (AID) and COVID-19. (1.) Pathogenesis of NLRP3 Inflammasome associated AID (gray): Inflammasome formation is induced by a variety of triggers. Activated NLRP3 subsequently drives caspase-1 activation. Caspase-1 mediates transformation from pro-IL-1β and pro-IL-18 to active IL-1β and IL-18. The positive feedback loop stimulates NF-kB. (2.) SARS-CoV-2 pathogenesis (white): SARS-CoV-2 can stimulate a hyperinflammatory immune response with epithelial cell-mediated production of reactive oxygen species (ROS). ROS can stimulate NF-kB and NLRP3. Both pathways (1. and 2.) result in increased cytokine levels with laboratory signs and clinical symptoms associated with hypercytokinemia. Abbreviations: SARS-CoV-2: severe acute respiratory syndrome coronavirus 2; COVID-19: coronavirus disease 2019; ROS: reactive oxygen species; NLRP3: (NOD)-like receptor protein 3; NF-kB: nuclear factor kappa B; IL: interleukin; CRP: C-reactive protein, ESR: Erythrocyte sedimentation rate, MAS: macrophage activation syndrome; CSS: cytokine storm syndrome.