The aim of our research activities is to describe and model the complex networks of genes that are controlling host susceptibility and response during an infection. For this, genetic diversity in populations of recombinant mouse inbred lines are being used to elucidate complex genotype-phenotype relationships and interaction networks after influenza A infection and in regulatory T cells, respectively.
Diseases in humans are caused by many extrinsic and intrinsic factors. One of the most important intrinsic determinant is genetic predisposition which can be very diverse and multi-factorial. Because of the complexity of the biological systems involved, these studies can only be performed in well-established experimental animal systems. Amongst the various animal models available, the mouse represents an ideal experimental system because its biology and genetics are very well characterized and powerful resources for systematic approaches are now available.
In particular, mouse genetic reference populations have been established that are inbred and thus genetically identical within a strain but differing in their genetic constitution between strains. Studying phenotypic variations in these populations allows to establish genotype to phenotype relationships enabling a systematic approach for the understanding of biological systems and mimicking human genetic diversity.
Our data can be associated with other genetic traits collected on the same genetic reference populations, and a multi-scale, multi-level network analysis of gene to phenotype correlations can be performed. This approach is referred to as Systems Genetics.
Genetic control of susceptibility towards influenza infections
Regulatory networks in regulatory T-Cells
You can find more information on the research group in these press releases and podcasts in German.
