Project B01 - Regulation of neutrophil recruitment by A20 in the fetus and in postnatal life
Premature infants are at high risk to develop life-threatening infections shortly after birth. This has been linked to their immature and functionally limited innate immune response. We have recently identified A20, a potent negative regulator of NF-κB signaling, as putative factor restricting innate immune responses in the fetus. Using in vivo and in vitro approaches as well as different genetic mouse models, we intend to clarify the role of A20 in innate immune cell trafficking not only during mouse and human fetal life but also in the adult organism.