D.V.M- School of Veterinary Medicine, Hannover, Germany
Ph.D. – School of Veterinary Medicine, Hannover, Germany
Peetz Family Professor, Department of Molecular Microbiology and Immunology, BSPH
Bloomberg Distinguished Professor of Immunology and Infectious Diseases
Departments of Molecular Microbiology and Immunology, BSPH, and Molecular and Comparative Pathobiology, SOM
Director, Lyme and Tickborne Diseases Research and Education Institute
615 N Wolfe Street, E4135
Baltimore, MD. 21205
Phone: (410) 614-2718
E-mail: [email protected]
Keywords: Immunity to infections; Host-pathogen interaction; B cell immunology; Influenza Virus infection; Lyme disease
The Baumgarth lab studies cellular and molecular mechanisms and signals that regulate B cell and B cell subset responses to infections. The objective of this research is to enhance our knowledge of how long-lasting protective immunity is induced. We study these responses mostly with mouse infection models, using tools such as multiparameter flow cytometry, transcriptomics, cell signaling, proximity ligation assays, ELISA, ELISPOT and protein chemistry.
One model we study is respiratory tract infection with influenza A virus that results in the establishment of highly effective, strongly protective and long-lived systemic and tissue-resident immunity. A particular emphasis of the lab has been the exploration of immediate early innate immune signals and how they shape the developing adaptive immune responses. We identified Type I IFN upregulation of endosomal toll-like receptors and the utilizing of both TRIF and MyD88 adaptor molecules as critical for maximal early B cell differentiation after influenza infection by integrating B cell receptor (BCR) and TLR-mediated signals. Ongoing studies are to explore the specific mechanisms by which these innate signals regulate effective B cell responses and how this affects the repertoire of the developing humoral responses.
The other is the study of infections with Borrelia burgdorferi, the causative agent of Lyme disease. In mice this tick-transmitted infection establishes persistence. The infection induces B cell responses that prevent disease but do not clear the infection in these natural reservoir species. We have identified multiple B cell response abnormalities that point to an active immune evasion/suppression of these adaptive immune responses by B. burgdorferi to achieve persistence. Our studies also identified a failure of effector CD4 T cell polarization during B. burgdorferi infection that we aim to further define at the molecular level. We are currently developing new mouse models to allow us and others to explore the molecular mechanisms underlying these failures of appropriate adaptive immune response induction.
Finally, we are interested in a fascinating, small innate-like fetal-derived subset of B cells, termed B-1, which generate much of the circulating IgM, but appears refractory to BCR stimulation. Our studies to-date have identified two distinct populations of natural IgM-secreting B-1 cells, terminally differentiated B-1 plasma cells, as well as an unusual fetal-derived B-1 cell that does not appear to terminally differentiate in order to secrete these antibodies. Our ongoing work is designed to better understand the regulation of these important antibody-secreting cells. We are also working on determining why effective IgG response induction requires both secreted IgM as well as its receptor on B cells, the FcR.
Publications and Interests:
Miller Research Building
733 North Broadway
Baltimore, Maryland 21205