Welcome to the homepage of the Division of Developmental Immunology (DDI) at the Biocenter of the Medical University of Innsbruck. The DDI is currently headed by Prof. Andreas Villunger, PhD, who was appointed as a head of this unit in 2007 as junior professor and is now full professor for Developmental Immunology at MUI.
The division is organized in four research groups, run by division head Andreas Villunger and associate professors Jan Wiegers, Verena Labi and Sebastian Herzog. Please click the logo to learn more about the respective group!
With their coworkers, DDI investigators explore basic mechanisms of immune cell development and differentiation with a focus on microRNAs and steroid hormones. In addition, we are interested in studying general principles of cellular transformation, focusing on the role of BCL2-regulated cell death and the p53 signalling network as barrier against malignant disease.
All group leaders are involved in training undergraduate as well as graduate students of different life-science disciplines, including biochemistry, biology as well as molecular and human medicine. If you are interested in research training opportunities at different levels (summer students, BSc, MSc, or MD/PhD), or have any teaching related questions, please contact Claudia in administration to organize an appointment with your group leader of interest (Claudia.Ram@i-med.ac.at).
Poster Prize for Gerlinde
On the recent 33rd Genes & Cancer Annual Meeting 2019 in Cambridge (UK), Gerlinde went all out and won the Poster Price sponsored by the FEBSJournal. Congratulations! This is pushing her even further to study the BCL-2 protein family in mitotic cell death & the maintenance of genomic stability.
DOC fellowship for Michael
In good tradition of the Division, Michael has recently received one of the prestigious DOC fellowships granted by the
Austrian Academy of Sciences. He will now proceed to unravel the diverse molecular mechanisms that underlie the regulated
processing of clustered microRNAs. Congratulations, Michael!
While CD4+ T cells are essential targets of glucocorticoids, it is not known whether these hormones also exert effects on CD4+Foxp3+ regulatory T cells. Here, Lourdes and Jan generated mice with a specific deletion of the glucocorticoid receptor (GR) in Foxp3+ Treg cells and demonstrate that these Tregs fail to prevent the induction of inflammatory bowel disease in vivo. These findings reveal that the GR is critical for Foxp3+ Treg cell function and suggest that endogenous glucocorticoids prevent Treg cell plasticity toward a Th1-like Treg cell phenotype in experimental colitis.
How GC B cells exert control over the DNA damage response while introducing mutations in their antibody genes is poorly understood. Here, Verena and here team show that the DNA damage response regulator Checkpoint kinase 1 (CHK1) is essential for GC B cell survival. In particular, they demonstrate that CHK1 inhibition or loss of one Chk1 allele impairs the survival of class-switched cells and curbs the amplitude of antibody production.