Dr. Stefanie N. Vogel, Ph.D.

Professor of Microbiology and Immunology

Dr. Stefanie Vogel received her Ph.D. from the University of Maryland, College Park in 1977 and then did postdoctoral research at the National Institute of Dental Research; Laboratory of Microbiology and Immunology, NIH under Dr. Joost Oppenheim where she characterized inheritance and mapped the Lps gene in macrophages and showed that interferons, and particularly endogenous IFN-b production by macrophages, contributed significantly to macrophage responses to bacterial products such as LPS.  In 1980, she began a 22 year academic career at the Uniformed Services University of the Health Sciences, Bethesda, MD where she rose to the rank of Professor.  In 2002, she joined the University of Maryland School of Medicine as Professor of Microbiology and Immunology and Professor of Medicine. Throughout her career, she has had continuous NIH grant support for her research (including an NIH Merit Award) and has received numerous invitations to speak on her current studies at many national and international meetings, including the NIH Immunology Interest Group, the American Association of Immunologists, the former ISICR, the International Endotoxin and Innate Immunity Society, the Society for Leukocyte Biology, and Toll Meetings. Her CV lists over 290 peer-reviewed publications, many in high impact journals, 37 book chapters and reviews and 5 patents. To date, she has mentored 35 post-doctoral fellows and 11 graduate students, and is currently director of a NIH Training Grant, Signaling Pathways in Innate Immunity.

Dr. Vogel’s research is focused on the capacity of macrophages to respond to bacterial products such as the endotoxic lipopolysaccharide (LPS) of Gram negative bacteria. Their studies on the role of Toll-like receptors (TLRs) in this process has led to the dissection of intracellular signaling pathways that define TLR responses to different pathogens, suggesting that these receptors have evolved to enable the host to respond appropriately to specific pathogens. In addition to examining the expression of a variety of proinflammatory genes and interferons as a consequence of exposure of macrophages to LPS and other microbial products, the Vogel laboratory is also actively studying mechanisms by which the inflammatory response to infection is controlled in mice and in humans. Specifically, they have utilized a paradigm of in vitro and in vivo “endotoxin tolerance”ˇ in which macrophages or mice exposed to a relatively low dose of LPS become transiently refractory to subsequent challenge to a variety of TLR agonists. An analysis of the kinase and DNA binding activities of signaling components involved in the TLR4 and TLR2 signaling pathways have been examined systematically by her group, in addition to studies that demonstrate dysregulated interactions among intracellular proteins required for this activation. This is best exemplified by work carried out by her group that identified the underlying genetic defect in a child with severe, recurrent bacterial infections as an IRAK4 deficiency. Lastly, the Vogel laboratory has also pursued mechanisms of inflammatory damage in many animal models where cytokines and IFNs figure centrally in disease progression, pathology, and resolution (e.g., stroke, encephalitic viruses, cecal ligation and puncture-induced polymicrobial sepsis, hemorrhagic shock, Respiratory Syncytial Virus (RSV) infection, and more recently, influenza infectoin). The work in the Vogel laboratory is highly translational: using TLR4 antagonists to block influenza-induced acute lung injury, the re-purposing of FDA-approved drugs that increase expression of M2 macrophages to resolve RSV-induced pathology, and development of a TLR2 antagonist using Computer Aided Drug Design to target a region within the TLR2 TIR domain, are all examples of her most recent efforts to apply our basic understanding of the role of cytokines and interferons to the resolution of diseases.