Welcome to the homepage of the Institute for Developmental Immunology (IDI) at the Biocenter of the Medical University of Innsbruck. The IDI 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 Institute is organized in four research groups, run by 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).
Checkpoint kinase 1 (CHK1) has developed into a promising drug target since tumor cells often depend on CHK1 function for survival. Here, Fabian and his colleagues
describe a previously unrecognized role for CHK1 in establishing and maintaining hematopoiesis.
Ten‐eleven‐translocation (TET) enzymes promote gene expression by catalyzing the oxidation of 5‐methylcytosine in DNA. In this publication that has recently been selected as Editor's Choice we show that TET function is vital for humoral immunity. TET activity guides the transition of germinal center B cells to antibody‐secreting plasma cells, and promotes antibody isotype switching. Loss of TET function favors C‐to‐T and G‐to‐A mutagenesis during somatic hypermutation, a finding of potential significance for the etiology of B‐cell lymphomas and other tumor entities.
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.
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.