Interleukin (IL)-33, a nuclear factor and a cytokine of the IL-1 family, has received a lot of attention in recent years because of its important role in chronic inflammatory and autoimmune diseases. It appears to be critically involved in the regulation of various physiological processes by influencing a wide range of immune cells. Previous reports and studies have primarily focused on the effects of IL-33 on traditional target cells, such as mast cells and type 2 innate lymphocytes. Dendritic cells (DC) are the most functionally specialized antigen-presenting cells that have been discovered to date. It has been demonstrated that IL-33 can activate DC via its specific receptor serum stimulation-2 (ST2), thereby regulating the host immune response and playing key roles in the pathogenesis of occurrence and progression of various diseases. The immune regulation of DC by IL-33 mainly involves signal pathways, such as NF-κB, p38 MAPK, and STAT1/3, in turn mediating the maturation, differentiation, and inflammatory response of DC. In addition, DC is an important source of the secretion of IL-33, which enhances the immune reaction and Th2 response through a positive feedback amplification loop. IL-33 activated DCs can promote tumor immunity and resist pathogen invasion, and also participate in the development of autoimmune and inflammatory diseases. This paper reviews the potential role and underlying mechanism of IL-33 in regulating DC immune response in order to provide a foundation for further research into its immune function and modulatory pathway in diseases.