Effect of Bisphenol a on the Immune Function of Dendritic Cells and T Cells

Degree: PhD
University: University of Leipzig , Faculty: Faculty of Medicine
City: Leipzig , Country: Germany
Discipline: Life Sciences, Medicine & Health
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  • Tuition fee Free - Details
  • Start Date of Studies Unknown
  • Admission deadline The positions are open until an appropriate candidate is found.
  • Language English
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  • Programme Description

    Programme Description

    The incidence and prevalence of allergic diseases has increased substantially in the last two decades. Environmental factors are thought to contribute significantly to this recent increase. Bisphenyl A (BPA) is a main xenoestrogen commonly used in the plastic industry and other by-products and pollutants. The risk of low-dose exposure to BPA for human health has been discussed controversially in the last years. Although the BPA uptake in humans seems to be safe, the risk assessment and exposure estimates in humans are not solid yet. Furthermore, recent data from animal studies suggest that endocrine disruptors such as BPA may affect the reproductive system and the immune system, especially after fetal or postnatal exposure. The central hypothesis to be examined is whether low dose BPA modulates immune responses important in allergy development via modulation of retinoid receptors or the arylhydrocarbon receptor (AhR). In utero exposure of BPA increased the expression of AhR, retinoid acid receptor RAR and RXR in cerebral and gonadal tissues. It is known that interaction of both, RAR and AhR, influences the development and effector functions of various immune cell types. Therefore, in this project the Phd student is challenged with the interdisciplinary work within the field of clinical allergology, basic immunology and ecological monitoring. In vitro investigations will analyse effects of BPA on retinoid receptors and AhR expression on human and murine immune cell and their phenotype and function. In vivo experiments will give information about whether fetal and postnatal exposure of mice to BPA lead to increased Th2 phenotype via altered expression of retinoid receptors or AhR on immune cells which promote development of allergic asthma or atopic eczema in the offspring.


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