Mechanisms in allergic skin disorders

Background Allergic skin disorders are initiated and maintained through the action and interaction between resident tissue cells, infiltrating leucocytes and mediators. Review The major cellular components of the skin immune system are keratinocytes, dendritic cells such as epidermal Langerhans cells (LCs) and dermal dendritic cells, mast cells and fibroblasts. Following an allergenic stimulus, inflammatory and immunocompetent cells accumulate in the epidermis and dermis, giving rise to specific clinical and histological manifestations. Leucocytes which accumulate in the inflammatory focus attract more leucocytes and stimulate the resident cell population. Primary mediators, released by resident cells upon stimulation, play a vital role in initiating and controlling inflammation. The mediators induce vascular endothelial cells to express adhesion molecules, which mediate migration of leucocytes into the dermis, where chemotactic factors attract them to the inflammatory focus. Activation of trapped T‐lymphocytes by antigen‐presenting cells (APCs) is followed by the release of inflammatory cytokines. Allergic contact dermatitis (ACD) depends on the activation of specifically sensitised T‐cells, and epidermal LCs are the primary APCs. Most contact allergens are small, chemically reactive moleculed and CD4 + Th1 type T‐cells are the target cells. Atopic dermatitis is a chronic eczematous condition, involving antibody IgE, LCs and dermal dendritic cells as the APCs, with Th2 T‐lymphocytes as the target cells. Urticaria comprises a heterogeneous group of conditions, characterised by a wheal and flare reaction. Mast cells are the principal source of mediators involved and histamine is the most important of these.