Atopic Eczema, Langerhans Cells and Allergy

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Abstract
While the pathomechanisms of respiratory atopy are rather well established, the role of IgE-mediated hypersensitivity in the elicitation and maintenance of eczematous skin lesions in atopic eczema is still controversial. Few diseases are characterized by an equally elevated production of IgE antibodies as atopic eczema. Many authors, however, regard this only as epiphenomenon. On the other hand, there is clearcut clinical evidence for exogenous elicitation of atopic eczema by contact with aero or food allergens. A variety of hypotheses may help to explain the participation of IgE antibodies in the induction of eczema: vasoactive mediators secreted by skin mast cells or basophils after allergen contact may produce itch, contact urticaria or a ‘late-phase-reaction’ with consequent eczematous skin changes further maintained by scratch responses. Recent investigations stress a possible role of Langerhans cells in the epidermis with a low affinity receptor for IgE with possible function for antigen presentation, mediator release or regulatory interactions. Certain cytokines such as interleukin-4 or gamma-interferon are able to enhance the expression of the IgE-receptor on the surface of Langerhans cells. IL-4 and gamma-interferon act synergistically in this respect on Langerhans cells, contrary to B cells. Furthermore lymphocytes may act directly via certain cytokines (e.g. histamine releasing factor, chemotactic factors etc.) on mast cells or eosinophil granulocytes in a proinflammatory sense. Eosinophils seem also to be involved in the inflammatory response in atopic eczema by releasing products such as major basic protein (MBP) or eosinophil cationic protein (ECP) which has been found to be elevated in severe atopic eczema. The role of other types of allergic reactions, as cytotoxic antibodies, immune complexes, IgG 4-antibodies as well as pseudo-allergic mechanisms is still controversial. There is some evidence for a possible elicitation of eczematous skin lesions by food additives in placebo-controlled challenge tests. Contact allergic responses seem to be similarly frequent in patients with atopic eczema compared to controls in an overall view; however, when regarded specifically, contact sensitization to metal salts, as nickel sulfate seem to be more frequent in atopies, while contact sensitization to other products, as lanolin, caines and other topicals, seem to be less frequent. The IgE antibodies found in patients with atopic eczema may be directed against aeroallergens (animal epithelia, dust mites), microbial antigens (staphylococci, pityrosporon) or food allergens. The clinical relevance of sensitizations against aeroallergens may be evaluated by an ‘atopy patch test’ which has to be further standardized before this procedure can be recommended for clinical routine. Diagnostic and therapeutic consequences include careful allergy diagnosis in patients with severe atopic eczema not responding to mild topical treatment. It is critical to differentiate between coincidence and relevance, i.e. each positive test reaction has to be evaluated carefully with regard to the possible clinical relevance for the eczematous skin lesions.

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