A model for regulation of dietary iron absorption by LP macrophages. During the starved state or following infection, the mTORC1 pathway remains inactive in LP macrophages (left). This allows proper localization of transferrin in the LP interstitium, which in turn promotes iron efflux from enterocytes via ferroportin. Activation of mTORC1 signaling in LP macrophages during the fed state induces expression of serine proteases that target transferrin for degradation (right). Absence of the iron (Fe) acceptor from the LP impairs iron efflux from enterocytes, despite high expression of ferroportin, and promotes its sequestration within ferritin.