IL6 and COVID-19: Despite evidence of impaired oxidative burst capacity in these neutrophils, the presence of neutrophil extracellular traps which may be regulated by interleukin-6, and their excessive activation in severe COVID-19 implicate a potential role in amplifying the inflammatory cascade and activating platelets to promote thrombosis.[13,30–32] Studies have shown that SARS-CoV-2 infection specifically induces an immune response in B cells.