Rate My Professor Hans Haecker

Hans Haecker, MD, PhD, is Professor of Microbiology and Immunology in the Department of Pathology, Division of Microbiology and Immunology at the University of Utah Spencer Fox Eccles School of Medicine. He received his MD from the University of Ulm, Germany, and his PhD as well as MD board certification in Microbiology and Infection Epidemiology from the Technical University Munich, Germany. He conducted postdoctoral training in the laboratory of Dr. Michael Karin at the University of California, San Diego School of Medicine, investigating Toll-like receptor signaling pathways and their roles in inflammation and host protection. From 2005 to 2019, he served as Assistant and Associate Member at St. Jude Children’s Research Hospital, expanding his research on TLR signaling in inflammation, autoimmune disease models, blood cell development including myelopoiesis, and drug discovery.

Since 2019, Dr. Haecker has been Professor at the University of Utah, where he serves as Associate Chief and Director of Graduate Studies in the Microbiology and Immunology Division, director of the Basic Immunology course, and co-chair of the Department Advisory Committee. He is a member of the Huntsman Cancer Institute Cell Response and Regulation program and the Center for Iron and Heme Disorders. As co-founder and board member of Nanospot.ai, he advances point-of-care diagnostics. His research centers on innate immunity and inflammation, encompassing molecular signaling mechanisms, immune cell differentiation, microbiota influences in inflammatory diseases such as systemic lupus erythematosus and psoriasis, hematopoiesis, and therapeutic drug development. Notable publications include "Specificity in Toll-like receptor signalling through distinct effector functions of TRAF3 and TRAF6" (Nature, 2006), "Patrolling monocytes promote the pathogenesis of early lupus-like glomerulonephritis" (Journal of Clinical Investigation, 2019), "Identification of Toll-like receptor signaling inhibitors based on selective activation of hierarchically acting signaling proteins" (Science Signaling, 2018), and "A phospho-tyrosine-based signaling module using SPOP, CSK, and LYN controls TLR-induced IRF activity" (Science Advances, 2022).