Allergic contact dermatitis (ACD) referred to as contact hypersensitivity (CHS) is one the most frequent inflammatory skin diseases characterized by redness, papules, and vesicles, followed by scaling and dry skin. ACD is elicited upon skin contact with non-protein chemicals called haptens and corresponds to a cutaneous delayed-type hypersensitivity reaction, mediated by hapten-specific T cells. During the sensitization phase, both CD4+ and CD8+ T cell precursors are activated in the draining lymph nodes by presentation of haptenated peptides by skin dendritic cells (DC). Subsequent hapten painting on a remote skin site induces the recruitment and activation of specific T cells at the site of challenge leading to apoptosis of keratinocytes, recruitment of inflammatory cells and development of clinical symptoms. Experimental studies from the last 10 years have demonstrated that, in normal CHS responses to strong haptens, CD8+ type 1 T cells are effector cells of CHS through cytotoxicity and IFNgamma, production while CD4+ T cells are endowed with down-regulatory functions. The latter may correspond to the recently described CD4+ CD25+ regulatory T cell population. However, in some instances, especially those where there is a deficient CD8 T cell pool, CD4+ T cells can be effector cells of CHS. Ongoing studies will have to confirm that the pathophysiology of human ACD is similar to the mouse CHS and that the CHS response to common weak haptens, most frequently involved in human ACD, is similar to that reported for strong haptens.
Apoptosis; Dermatitis, allergic contact; Inflammation; Skin
