Although neutrophils are typically considered poor antigen-presenters, our findings suggest that, similar to what we observed in circulating myeloid cells, ‘active’ neutrophils in the lungs of critical COVID-19 patients have further lost antigen-presenting capacity and have adopted a deleterious phenotype that contributes to inflammatory cytokine signalling (IL1B, CXCL8, NEAT1) and local tissue damage (FPR1). The gene discussed is IL1B; the disease is COVID-19.