[Immunologic basis of allergic contact eczema].

Allergic contact dermatitis is an inflammatory skin disorder induced by low molecular and reactive haptens (contact allergens) coming into contact with the skin of sensitized individuals. The sensitization or induction phase is characterized by an activation of allergen-specific T-effector lymphocytes. For proliferation and differentiation of these cells presentation of hapten, associated with Ia-molecules on the surface of Langerhans cells, is required. Further activating and modulating signals are delivered by interleukin 1, interleukin 2, interferon, prostaglandins and some more. The activation and function of the T-effector cells is controlled by T-suppressor lymphocytes. Antibody, in particular antiidiotype antibody, can be regulators of this cell-mediated immune response. The effector phase is characterized by a reaction of the T-effector lymphocytes with the eliciting allergen: this results in a secretion of lymphokines. Lymphokines attract and activate other cells such as macrophages, lymphocytes, neutrophile and basophile leukocytes. These cells release inflammatory mediators.