Allergic contact dermatitis (ACD) to haptens can serve as a valuable paradigm for understanding the physiopathology of T cell mediated immune responses. In sensitized individuals, exposure to the relevant hapten initiates clinical expression of ACD, which depends on the rapid activation of specific T cells. Mechanisms of tissue damage include direct cytotoxicity against keratinocytes, mostly mediated by CD8⁺ T cells, and T cell release of cytokines, which amplify the inflammatory response by targeting resident skin cells. The expression of ACD is actively regulated by specialized subsets of T lymphocytes with suppressive functions. In particular, T regulatory cells producing high levels of IL‐10 suppress ACD by blocking the functions of dendritic cells. In contrast CD4⁺CD25⁺ regulatory T cells prevent immunopathological reactions and maintain peripheral tolerance to haptens by acting via a cell‐to‐cell contact mechanism. Understanding the role of suppressor T cells and the requirements for their in vivo and in vitro expansion are critical steps for the development of specific desensitization protocols in hapten‐allergic individuals. This information may also provide the basis for novel interventions in other immune‐mediated diseases.