Our findings suggest that in severe COVID-19, DCs, and in particular the cDC2 lineage, are immature with alterations in the developmental phenotype, lack up-regulation of the activation marker CD38, as seen in moderate patients, and lose the inhibitory receptor CD200R, all possibly contributing to inefficient regulation of proinflammatory conditions in severe COVID-19. The gene discussed is CD200R1; the disease is COVID-19.