The cooperation of allergens via induction of cytokines secretion in the inflammed tissue can influence to the reactivity of peripheral blood mononuclear cells (PBMC). Using an Elispot method the cytokines profile of PBMC stimulated with nickelsulfate (NiSO4), D1 antigen (a.D1) of Dermatophagoides pteronyssinus and staphylococcal enterotoxins (SEA, SEB) in vitro in an acute and chronic phases of atopic dermatitis (AD) and in controls (healthy volunteers) was investigated. It was concluded: Nickel is supposed to participate in the pathogenesis of contact allergy to nickel inAD as an superantigen. The result of patch test to nickel may not always inform about the presence of nickel-sensitive cells in the blood circulation. The contact allergy to nickel via the promotion of Th1 mechanisms is supposed to inhibit a house dust mite allergy related to Th2 mechanisms appearing when the concentration of a. D1 arises. The contact allergy to nickel and the cross-reactivity of nickel in food allergy, and the decrease of IFNg secretion in the circulation may be related with the skin infection of S. aureus in AD. In the remission of AD the predominance of Th1 mechanisms was observed when high IgE concentration was found. The accompaniance of allergic asthma and contact dermatitis with AD is supposed tomodify the mechanisms related with the response of PBMC to a.D1, SEA, SEB,NiSO4 in AD.