The SARS-Cov2 infection triggers a multisystem inflammatory disorder, knowing as COVID-19, a pandemic disease. This disease is characterized by acute respiratory distress syndrome, cytokine-driven hyperinflammation, and leukocytes count changes. The innate immune response has been linked to COVID-19 immunopathogenesis (e.g., dysfunctional IFN response and myeloid inflammation). In this regard, neutrophils have been highlighted as essential effector cells in the development of COVID-19. This review summarized the significant finds about neutrophils and its effector mechanisms (e.g., neutrophils enzymes and cytokines, neutrophil extracellular traps) in COVID-19 so far.
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【저자키워드】 Inflammation, SARS-CoV2, chemokines, NETs, 【초록키워드】 COVID-19, Cytokines, innate immune response, Neutrophil extracellular traps, neutrophil, Infection, hyperinflammation, Immunopathogenesis, disease, acute respiratory distress, Inflammatory, IFN response, Trigger, leukocyte, changes, enzyme, syndrome, pandemic disease, disorder, Effector mechanism, characterized, effector cell,
【저자키워드】 Inflammation, SARS-CoV2, chemokines, NETs, 【초록키워드】 COVID-19, Cytokines, innate immune response, Neutrophil extracellular traps, neutrophil, Infection, hyperinflammation, Immunopathogenesis, disease, acute respiratory distress, Inflammatory, IFN response, Trigger, leukocyte, changes, enzyme, syndrome, pandemic disease, disorder, Effector mechanism, characterized, effector cell,