SUMMARYDysfunction in a wide variety of cellular immune mechanisms occurs in atopic dermatitis and contributes to the clinical presentation of the condition.The increased incidence of cutaneous viral and fungal infections, observed clinically in atopic dermatitis, suggests altered T‐lymphocyte function and elevated serum IgE levels suggest deregulation of B‐lymphocyte function. The clinical features of pruritus and erythema raise the possibility of increased release of inflammatory mediators into the circulation. In vitro studies have confirmed abnormalities in T‐lymphocyte subset numbers and function as well as increased releasability of histamine from blood basophils in atopic dermatitis.Recent studies have revealed abnormalities in the metabolism of cyclic AMP, an important mediator in cellular regulatory mechanisms, in atopic dermatitis. Leucocyte cyclic AMP responses to a variety of agonists are blunted in atopic dermatitis and are due, at least in part, to increased cyclic AMP phosphodiesterase activity. It is unclear at present whether this enzyme abnormality is genetically determined or whether it is induced by increased circulating levels of inflammatory mediators. A number of the in vitro abnormalities in atopic dermatitis appear to correlate with the increase in phosphodiesterase activity.Further research aimed at finding ways to inhibit phosphodiesterase activity in atopic dermatitis and consequently reversing other abnormalities in cellular function, will hopefully open up new avenues of therapy for this common and disabling cond