Abstract
There is strong evidence that COVID-19 pathophysiology is mainly driven by a spatiotemporal immune deregulation. Both its phenotypic heterogeneity, spanning from asymptomatic to severe disease/death, and its associated mortality, are dictated by and linked to maladaptive innate and adaptive immune responses against SARS-CoV-2, the etiologic factor of the disease. Deregulated interferon and cytokine responses, with the contribution of immune and cellular stress-response mediators (like cellular senescence or uncontrolled inflammatory cell death), result in innate and adaptive immune system malfunction, endothelial activation and inflammation (endothelitis), as well as immunothrombosis (with enhanced platelet activation, NET production/release and complement hyper-activation). All these factors play key roles in the development of severe COVID-19. Interestingly, another consequence of this immune deregulation, is the production of autoantibodies and the subsequent development of autoimmune phenomena observed in some COVID-19 patients with severe disease. These new aspects of the disease that are now emerging (like autoimmunity and cellular senescence), could offer us new opportunities in the field of disease prevention and treatment. Simultaneously, lessons already learned from the immunobiology of COVID-19 could offer new insights, not only for this disease, but also for a variety of chronic inflammatory responses observed in autoimmune and (auto)inflammatory diseases.
Highlights
Coronavirus Disease-2019 (COVID-19) has costed millions of lives worldwide
Lessons learned from the immunopathology of COVID-19 hitherto, including the interplay between innate and adaptive immune responses, the immunemediated thrombosis, panoptosis, autoimmunity and cellular senescence, could offer new insights, for the disease per se, and for a variety of chronic inflammatory responses observed in autoimmune andinflammatory diseases
We have recently showed that SARS-CoV-2 triggers senescence with various clinical and epidemiological implications, including quasispecies generation [31]
Summary
Coronavirus Disease-2019 (COVID-19) has costed millions of lives worldwide. Since the beginning of the pandemic, the scientific community has joined forces to understand the pathophysiology of the disease, aiming to develop effective preventive and therapeutic measures. Peripheral blood neutrophils of severe COVID-19 patients show increased numbers and marked hyper-responsiveness, as attested by the enhanced degranulation, neutrophil extracellular traps (NETs) release and pro-inflammatory cytokine production [94].
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