Gitta Stockinger group project:

Modulation of immune responses by the aryl hydrocarbon receptor

The aryl hydrocarbon receptor (AhR) is a ligand dependent transcription factor best known for mediating the toxicity of dioxin. We showed that in the CD4 T cell lineage AhR expression is restricted to the Th17 subset. Activation of AhR during Th17 development markedly increases the proportion of Th17 T cells and it essential for their production of IL-22.

Activation of AhR by a potentially diverse range of endogenous and exogenous ligands is therefore an essential co-factor in the optimal differentiation of Th17 effector cells. The AhR links the biological activity of these cells- from their role in host defense to the detrimental role in autoimmunity- to a wide range of environmental factors. Furthermore, AhR has distinct physiological roles in other cell types, notably antigen presenting cells.

We are using Cre-mediated deletion and reporting for AhR expression in different cell types to study AhR impact in various inflammatory models in vivo.

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