Allergic Contact Eczema and Atopic Eczema

Abstract

Since Landsteiner and Chase used cell transfer experiments to demonstrate that the potential of eliciting allergic contact eczema resides in the mononuclear cell fraction of leucocytes, one must regard the allergic contact eczema as a manifestation of delayed-type hypersensitivity (DTH) [1, 2]. Later on, several other groups showed that the induction and elicitation of allergic contact eczema requires a complex interaction of multiple components. Various T-lymphocyte subpopulations and their products react with antigenpresenting cells which express HLA II antigens on their surface. In the epidermis, these are the Langerhans cells [3]. The sensitization phase includes the generation of T-helper and various types of regulatory T-suppressor lymphocytes which are specifically sensitized by per-cutaneously penetrating molecules of low molecular weight [4, 5]. The specificity is carried by CD4+ T-helper cells, as proven for nickel sensitivity [6]. After sensitization has occurred, any further cutaneous contact with the allergen will provoke the manifestation of an allergic contact eczema [7]. Immunologically, this represents the effector phase of cell-mediated immunity (CMI). Several investigators suggest a biphasic development of allergic contact eczema and consider the first part a mandatory prerequisite of the second. Within 4 h after contact with antigen, basophils which have been activated by T-cell factors invade the skin [8]. This specific “cutaneous basophil hypersensitivity” [9] is followed by an invasion with mononuclear cells, the vast majority of which are T cells without antigen specificity. It appears that a single antigen-specific helper cell is sufficient to initiate this late classic effector phase [10]. During this late phase of allergic contact eczema the kinetics of emigration and the phenotypic composition of the infiltrating cells cannot be distinguished from an irritant dermatitis [11].