ABSTRACT
Recent investigations have greatly increased our understanding of immunological mechanisms involved in the pathogenesis of atopic dermatitis (AD) (Fig. 1). The mononuclear cellular infiltrate in lesional skin of AD is mainly constituted of CD4+ T cells and to a lesser extent CD8+ T cells. T cells are activated by aeroallergens, food antigens, autoantigens and bacterial superantigens in AD. They are under the influence of skin-related chemokine network and they show skin-selective homing. Epidermal Langerhans cells and dermal dendritic cells are able to activate allergenspecific T cells through allergen-specific IgE-antibodies bound to Fc receptors for IgE (FcεRI and FcεRII). This leads to continuous stimulation of T cells in the skin. T cells play important roles in AD with induction of hyper IgE, eosinophil survival. In addition activated T cells induce keratinocyte apoptosis as a key pathogenetic event in the formation of eczema. To mediate these effector functions after skinspecific homing, activated T cells show continuous survival in the skin. Apoptosis of activated T cells (activation-induced cell death) is prevented by cytokines and extracellular matrix components in the eczematous skin.
