ABSTRACT
Atopic dermatitis (AD) is a chronic inflammatory skin disease clinically and histologically highly similar to allergic contact dermatitis (20, 41). Because of this similarity, the putative pathophysiological relationship between classical IgE-mediated allergic reactions occurring in atopic individuals, i.e., allergic rhinitis and allergic asthma bronchiale, and eczematous skin lesions in AD remains elusive. Our current understanding of allergic reactions in the skin, particularly in the field of eczematous skin diseases, implies that this kind of cellular infiltrate, mainly composed of T cells, has to be initiated and/or sustained by antigen-presenting cells (APC). As a rule, T cells require efficient stimulation by APC in order to become effector cells and to be implicated in a pathophysiological process. Thus, it is assumed that APC play a key role in driving the inflammatory reaction in AD lesions (8). Recently, it has been proposed to subdivide AD into two distinct forms: the “extrinsic” or “allergic” form (occurring in the context of sensitization toward environmental allergens) and the “intrinsic” or “nonallergic” form (occurring in the absence of any typical atopical background) (61). Based on the above, APC should be involved in both forms of AD. In this chapter we will focus on the role of professional APC, i.e., monocytes and dendritic cells (DC), including epidermal Langerhans cells (LC), since most progress has been made in recent years in understanding the putative role of these APC in the extrinsic/allergic form of AD.
