Atopic dermatitis (AD) is a chronic inflammatory dermatosis due to the activation ofT-cell lymphocytes specific to protein antigens in the skin. The AD antigens come from molecules in the environment (extrinsic AD allergens associated with hyper IgE levels) or from self antigens (intrinsic AD autoantigens). The physiopathology of AD implies dendritic cells, specific T-cell lymphocytes, a network of type 1 and 2 cytokines and inflammatory chemokines. Extrinsic AD is the best known because of the existence of animal models and skin tests with allergens in humans (atopy patch tests), which reproduce eczema lesions. Although the role of the penetration of pneumo-allergens, prompted by abnormalities in the skin barrier, in inducing AD flares is established, recent works suggest that other types of allergens (trophallergens) and/or proteins derived from micro-organisms may be responsible in some patients. The ongoing studies on animal models of AD will no doubt permit rapid progression in our knowledge of the mechanisms involved in the origin of the disease and the reasons for its progressive increase in frequency.