Dendritic cells are unique heterogenous cell population capable of responding to different inflammatory signals. These signals induce the process of maturation forcing cells to leave the inflamed site and to migrate to draining lymph nodes. During this process, dendritic cells have to initiate differentiation responses expressed among others by up-regulation of some surface antigens (e.g., MHC or costimulatory molecules) and down-regulation of the others (e.g., E-cadherin). There are more and more data published indicating that chemical compounds known to initiate contact hypersensitivity (haptens) can also induce the process of dendritic cells maturation resembling in some aspects their maturation after contact with common inflammatory factors. Although molecular events associated with the process have not yet been dearly defined, there is growing evidence that haptens mediate activation of dendritic cells by activating mitogen-activated protein kinases, mainly p38 MAPK. It may be speculated that further downstream signals include activation of transcription factors such as nuclear factor kappa-B (NF-kappaB), activating transcription factor-2 (ATF-2) or cAMP response element-binding protein (CREB). The present review will focus on some aspects of signal transduction pathways in dendritic cells stimulated with contact sensitizers.