Analysis of drug-specific cytokine production by means of flow cytometry proved a useful and reliable approach for the in vitro detection and characterization of drug hypersensitivities.

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Allergic reactions to drugs belong to the group of B-reactions, which are characterized not only by the pharmacologic profile of the drug but also by individual risk factors. Pharmacogenetic approaches facilitate identifying these risk factors. The most important example for Caucasian patients is NIDR (non-immediate drug reaction) to abacavir. Chinese patients possess risk factors for NIDR to allopurinol and anticonvulsants and the HLA locus on chromosome 6. Another potentially important area is assessing risk factors to prevent allergic reactions to antibiotics, especially with regard to the effective treatment of MRSA.

To understand the mechanisms involved in immunological tolerance to skin-associated proteins, we have developed trangenic (Tg) mice that express a model self antigen, membrane-bound ABSTRACTS 125 FS01.3 Disperse (yes), orange (yes), 3 (no): what do we test in textile dye dermatitis?Para-phenylenediamine (PPD), an arylamine dye, is a strong allergen causing allergic contact dermatitis. Cytokines such as TNF-a and IL-1beta are key mediators in the initiation of this reaction. Both cytokines are predominantly produced by stimulated monocytes and macroghages. We investigated the responses of PPD and Bandrowski's base (BB), an autoxidation product of PPD in human monocytes. We isolated monocytes from healthy volunteers and incubated them with the allergens. TNF-a and IL-1beta mRNA expression and protein levels were estimated after 45 min, 2 h, 4 h and 24 h after allergen contact. IL-1beta and TNF-alpha were measured in cell culture supernatants by ELISA (n ¼ 7) and mRNA expression was determined by real-time RT-PCR. We found that PPD reduced TNF-a protein secretion by 20-69.9% (n ¼ 6). Further, IL-1beta levels were decreased by 44-98%. The same tendency was found studying IL-1beta and TNF-a mRNA steady state levels (n ¼ 3; 1 h incubation). These effects were substance-specific and not found for PPD derivatives nor for the autoxidation product BB. These findings suggest that PPD may specifically modify immune responses by directly infering with the cellular proinflammatory cytokine network.

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