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The inflammatory milieu in human skin affected by chemical contact allergens
Project
Project code: BfR-PRS-08-1322-547
Contract period: 01.03.2013
- 31.12.2013
Purpose of research: Applied research
Allergic contact dermatitis (ACD) is a highly prevalent skin disease with up to 20% of individuals affected. ACD is often caused by occupational contact to sensitizing substances like dyes, resins or pesticides. It therefore constitutes not only a major individual burden but also negatively affects health systems and economy. So far, only unspecific immunosuppressant drugs like glucocorticoids are available for therapy. Specific cure remains elusive as many of the molecular mechanisms underlying ACD pathogenesis are still unknown.
ACD is caused by an overreaction of the immune system to small chemicals like Nickel, p-phenylenediamine or methyl methylacrylate. Skin contact with these sensitizers elicits an innate inflammatory immune response and – in susceptible individuals – a subsequent adaptive immune response. Recurrent antigen contact leads to the secretion of proinflammatory cytokines by the innate arm of the immune system and to the migration of adaptive effector T cells to the site of chemical contact. Therefore, both innate and adaptive immune defence mechanisms contribute to ACD pathogenesis.
With this project, we aim to analyze the inflammatory milieu of ACD skin models in order to characterize the molecular mechanisms of ACD and to identify new ACD biomarkers. To achieve this, we will work with patient skin samples which represent the best available model system. Only in human tissue samples, all relevant processes will surely be repre-sented. We will employ state of the art technology like next generation transcriptome se-quencing, real-time PCR analysis and confocal microscopy to characterize the molecules directly involved in the allergic reaction and to conclude on the molecular mechanisms that may underlay disease pathogenesis.
Section overview
Subjects
- Toxicology
