No abstract

Our results suggest that prophages (possibly animal-associated) have conditioned bacterial adaptation and ability to cause infections in neonates and adults, and support a role of lysogeny with the emergence of GBS as a pathogen in human.

Highlights d Vitamin D induces DNA demethylation at VDR binding sites in dendritic cells (DCs) d Differentiation to tolerogenic DCs associates with IL-6-JAK-STAT3 pathway activation d VDR, STAT3, and TET2 interact with each other in tolerogenic DCs d Pharmacological inhibition of JAK2 reverts vitamin D-induced DC tolerogenesis