RANKL-RANK interaction in immune regulatory systems

Figure 1 Modulation of dendritic cell functions by receptor activator of NF-κB ligand signaling. Receptor activator of NF-κB ligand (RANKL) signaling promotes the survival of conventional dendritic cells (cDCs) and ensures T cell priming and activation, thereby enhancing the acquired immune response (left). CD40 signaling may have a redundant role in this function of RANK signaling. In skin and, most likely, the intestines, RANKL-treated DCs maintain the number of Foxp3-positive regulatory T cells to suppress the immune response against self-antigens, food and commensal flora (right). In the skin, inflammation and ultraviolet (UV)-irradiation upregulate the expression of RANKL in keratinocytes.