Priv.-Doz. Dr. Rer. Nat. Caspar Ohnmacht

Caspar Ohnmacht obtained his PhD 2009 from the Ludwig-Maximilians-Universität München where he focused on innate type 2 immune effector cells such as dendritic cells, basophils and eosinophils in the lab of Prof. Daivd Voehringer. In 2010, he joined the lab of Prof. Gérard Eberl at the Institut Pasteur in Paris, France, where he discovered a novel type of regulatory T cells that is now accepted as a major cell type for the tolerization of intestinal bacteria. In 2013, he joined the Institute of Allergy Research at Helmholtz Munich where he became principal investigator of the Mucosal Immunology group. With the help of an ERC Starting grant, his current work focus on the cellular networks, the molecular networks and microbial factors that control the size and the function of this microbiome-induced regulatory T cell population and how this knowledge can be exploited for therapeutic approaches in inflammatory bowel diseases and allergic disorders. The Ohnmacht lab also seeks to identify the role of mesenchymal cells such as intestinal stromal cells to define the intestinal tract as an overall highly tolerogenic organ.

In an additional project, the Ohnmacht lab is also interested in the so-called ‘red meat allergy’ and the role of the environment, e.g. the intestinal microbiome, in the tolerization of the sugar epitope alpha-Gal. Indeed, by generation of a novel anti-alpha-Gal antibody, the work of his group has recently challenged the hypothesis that the intestinal microbiome is a major alpha-Gal source.

Together with Dietmar Zehn from the Life Sciences department at the TUM, he also uses gnotobiology as a highly controllable system and the LCMV infection model to study whether and how the intestinal microbiome influences anti-viral immunity and immunopathology.

Lastly, the Ohnmacht lab also investigates the role of the environmental sensor Aryl hydrocarbon receptor (AhR) in the context of allergic airway inflammation. For instance, the group could recently show together with Francesca Alessandrini that the absence of the AhR and some of its immediate downstream target enzymes of the CYP1 family results in aggravated lung inflammation.