The pathogenesis of allergic contact dermatitis (ACD) is very complicated. However, new discoveries have been made on the topic in recent studies. Epidermal keratinocytes not only promote T cell infiltration, but also limit the development of ACD. In addition, cutaneous dendritic cells possess both antigen presenting function and immunomodulatory activity. Furthermore, some immune cells and molecules have been newly demonstrated to be involved in the pathogenesis. For example, CD4+ CD25+ Foxp3+ T cells play a powerful immunosuppression role; T helper 17 (Th17) cells mediate and enhance inflammation reaction; B10 cells play a negative regulatory effect via an interleukin (IL)-10-dependent mechanism. Some adhesion molecules and their ligand (such as PSGL-1), as well as chemokines (such as CCL21) also exert a certain role in the pathogenesis of ACD.