At present, the induction and elicitation of an allergic contact dermatitis (ACD) with potent contact allergens such as diphenylcyclopropenone appears to be the most effective, but still not definitively curative, approach to treat extensive forms of alopecia areata (AA). Experimental data suggest that cytokines and growth factors such as IL-1 beta are involved in the pathogenesis of AA as well as the therapeutic effect mediated by contact sensitizers. It seems reasonable to assume that factors inherent in the late phase of ACD modulate a T-cell mediated mechanism responsible for AA, thus inducing hair regrowth. Such counteracting activities are most likely mediated by proinflammatory cytokines such as TNF-alpha, IL-10, or TGF-beta 1. This hypothesis may oversimplify the underlying immunological mechanisms, but the effectiveness of topical immunotherapy in AA would be compatible with this concept. This mode of treatment is, however, a rather rough approach and recurrences are possible. Hopefully, advances in basic science will eventually allow us to find a more specific mode of treatment.