Pathophysiological characteristics of these two types of eczema, both involve antigen specific effector T lymphocytes and down-regulatory CD4+ T cells (Treg). These cells are responsible for the cutaneous inflammatory response through the production of inflammatory cytokines and the destruction of keratinocytes by apoptosis. The main difference between these two types of disease is the nature of the environmental antigen. Indeed, protein allergens are involved in cases of atopic dermatitis whereas non protein chemicals (calles haptens) are responsible for allergic contact dermatitis. The skin lesions of eczema follow the activation of antigen specific T lymphocytes within the skin, leading to the production of inflammatory cytokines and to the destruction of keratinocytes by apoptosis. CD4+ Treg cells are endowed with down-regulatory and tolerogenic functions since they limit the skin inflammation in patients and prevent sensitization and induction of eczema in normal individuals. Eczema should therefore be considered as inflammatory dermatoses caused by the loss of immune tolerance to environmental antigens. Different strategies capable of restoring immune tolerance could avoid eczema outbursts and/or induce prolonged remissions of the disease.