ABSTRACT

Allergic contact dermatitis (ACD) and contact hypersensitivity (CHS) are delayed-type hypersensitivity reactions which are mediated by hapten specific T cells. During the sensitisation phases, both C D 4+ and C D 8 + T cell precursors are activated in the drain­ ing lymph nodes by presentation o f haptenated peptides by skin dendritic cells. Subsequent hapten skin painting induces the recruitment of T cells at the site of challenge which induce inflammatory signals and apoptosis of epidermal cells, leading to the development o f a skin inflammatory infiltrate and of clinical symptoms. There have been major controversies on the respective role of CD 4+ and C D 8 + T cells in the development o f the CHS inflammatory reac­ tion. Experimental studies from the last 10 years have demonstrated that, in normal CHS responses to strong haptens, C D 8 + type 1 T cells are effector cells o f CHS while C D 4+ T cells are endowed with down-regulatory functions. The latter may correspond to the recendy de­ scribed CD 4+CD25+ regulatory T cell population. However, in some instances, especially those where there is a deficient C D 8 + T cell pool, CD 4+ T cells can be effector cells o f CHS. Ongo­ ing studies will have to confirm that the pathophysiology of human ACD is similar to the mouse CHS and that the CHS response to weak haptens, the most frequendy involved in human ACD, is similar to that reported for strong haptens.