Jörn Coers, PhD – Biography
Director, Center for Host Microbial Interactions
Jörn Coers received his M.Sc. degree in Biology from the University of Konstanz, Germany in 1999. While enrolled at the University of Konstanz, Dr. Coers conducted his M.Sc. thesis work in Craig Roy’s laboratory at the State University of New York, Stony Brook and later at Yale University where he continued to work as a research assistant until the spring of 2000. Dr. Coers made several important findings during his two and a half year stint in the Roy lab including the discovery of a chaperone complex in the bacterial pathogen Legionella pneumophila that is essential for the injection of virulence factors into host cells.
For his doctoral training, Dr. Coers employed transgenic mouse models to study the role of cytokine signaling in hematopoiesis at the German Cancer Research Center and at the University of Basel, Switzerland, in the laboratory of Radek Skoda. His work led to the discovery that aberrant expression of the thrombopoietin receptor protein can cause thrombocytosis due to a shift in the balance between thrombopoietin-induced proliferation of platelet precursor cells and removal of thrombopoietin by receptor mediated internalization in platelets.
For his postdoctoral training, he returned to the topic of host-pathogen interactions and applied his knowledge of mouse genetics to study infectious disease in the labs of Bill Dietrich and Michael Starnbach at Harvard Medical School. He identified members of a large family of Interferon-inducible GTPases as critical components in the innate immune response to the bacterial pathogen Chlamydia trachomatis, the cause of a common sexually transmitted disease resulting in sterility and the leading cause of preventable blindness globally.
In 2010, Dr. Coers began his independent laboratory as an Assistant Professor in the Department of Molecular Genetics and Microbiology at Duke University Medical Center. His laboratory is interested in the fundamental aspects of immune recognition of intracellular bacterial pathogens and the corresponding microbial counter-immune strategies. His lab uses applied genetic approaches in mice and mammalian cell lines to identify novel host genes required for innate immune responses and bacterial genetics to identify key bacterial genes involved in triggering or evading host immunity.