Postnatal monocyte maturation requires age-dependent initiation of regulatory gene programs when losing birth-associated stress tolerance. Homo sapiens

We disprove that the impaired Myd88-dependent proinflammatory response of neonatal monocytes is a correlate for immaturity and confirm it as display of transient alarmin-mediated stress tolerization. We find a strong inducibility of TRIF-dependent genes in neonatal monocytes by LPS but a barely detectable expression at baseline. Overall design: Isolated adult blood (AB) and cord blood (CB) monocytes were stimulated for 4h with lipopolysaccharide (LPS).