The deciphering of the immune cells and marker signature in COVID-19 pathogenesis: An update

The precise interaction between the immune system and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is critical in deciphering the pathogenesis of coronavirus disease 2019 (COVID-19) and is also vital for developing novel therapeutic tools, including monoclonal antibodies, antivirals drugs, and vaccines. Viral infections need innate and adaptive immune reactions since the various immune components, such as neutrophils, macrophages, CD4(+) T, CD8(+) T, and B lymphocytes, play different roles in various infections. Consequently, the characterization of innate and adaptive immune reactions toward SARS-CoV-2 is crucial for defining the pathogenicity of COVID-19. In this study, we explain what is currently understood concerning the conventional immune reactions to SARS-CoV-2 infection to shed light on the protective and pathogenic role of immune response in this case. Also, in particular, we investigate the in-depth roles of other immune mediators, including neutrophil elastase, serum amyloid A, and syndecan, in the immunopathogenesis of COVID-19.

Automated summary

The interaction between the immune system and SARS-CoV-2 is crucial for understanding COVID-19 pathogenesis and developing therapeutic tools. Different immune components play various roles in viral infections, and characterizing the immune reactions is essential for defining the pathogenicity of COVID-19. Furthermore, investigating the roles of other immune mediators in the immunopathogenesis of COVID-19 is necessary.