Nicole Baumgarth, DVM, PhD


SVM: Pathology, Microbiology & Immunology
Center for Comparative Medicine
University of California, Davis
Davis, CA 95616
Office: (530) 754-5813
Lab: (530) 754-5813
Fax: (530) 752-7914

Research Interests:

The Baumgarth Lab investigates the basic immunological mechanisms that regulate and control immunity to pathogens. They aim to reveal the signals that drive a protective B cell response and to determine how these responses might be derailed by certain pathogens. Two mouse models of infection are being studied: influenza virus and Borrelia burgdorferi, the Lyme Disease agent. They are interested also in understanding the development and the role and function of a small innate-like B cell subset, termed B-1 cells and the natural IgM this subset is producing.

Research tools: We primarily use mouse-models to study the regulatory processes controlling successful and unsuccessful immune responses. We breed numerous genetically engineered mice that help us to dissect specific aspects of the immune response. Much of our work relies on in vivo and ex vivo analyses tools such as multiparameter flow cytometry for functional and phenotypic studies, histology and immunohistochemistry, ELISA, ELISPOT, Laser-dissection microscopy, microarray/RNAseq and qRT-PCR analysis and other state-of-the-art cellular and molecular immunological assays.

Collaborators: Our studies are conducted in collaboration with Drs. Stephen Barthold (CCM, UC Davis), Scott Simon (UC Davis, Biomedical Engineering), Frances Lund, Troy Randall and Allan Zajac (University of Alabama, Birmingham) and Eun-Frances Lee and Inaki Sanz (Emory University). We also work with Northrup Gruman and the J. Craig Venter Institute to enhance the utility of the Influenza Research Database (, a NIH-supported web-based database for influenza research.

Disease Models: We use two mouse infectious disease models for our studies: Infections with influenza virus and infections with Borrelia burgdorferi, a bacterial spirochete and the causative agent of Lyme disease. The influenza infection models serve as an outstanding example of a highly successful B cell response, which we can use to identify the innate and adaptive immune regulators that control the induction and maintenance of highly protective responses. In contrast, following infection with Borrelia burgdorferi, an immune response is induced, but the bacteria cannot be cleared. We find great abnormalities in the B cell response, most importantly, a lack of long-term adaptive immunity. We hope to understand the reasons for this lack of long-term immune induction. Furthermore, we are probing the CD4 T cell responses to this pathogen to determine whether these responses are also affected.

Innate-like B cells: While T and B cells are a central part of the adaptive immune system, a small subset of B cells, termed B-1 cells, is considered an “innate-like” lymphocyte, because it expresses aspects of the adaptive immune system (an antigen-receptor that relies of gene-rearrangement) and the innate immune system (rapid responses to innate signals, a BCR that responds to pathogen-associated molecular patterns). These cells contribute nearly all of the protective natural IgM antibodies that are constitutively generated in mice, independent of whether the mice were infected or not, or whether they were colonized with bacteria in their gut and on mucosal surfaces, or are held under sterile conditions. We are interested in identifying the mechanisms by which these B cells generate antibodies without stimulation by foreign antigens. We are also interested in identifying the functions of IgM during influenza infection and during infection with B. burgdorferi that are unique to this type of antibodies by their interaction with specific IgM-recognizing receptors.

Luo, Jean


Nguyen, Trang

Graduate Student (Grad Group Immunology)

Olsen, Kimberly


Ram, Shivneel

Junior Specialist

Savage, Hannah

Graduate Student (DVM/PhD dual degree)

Tracy, Karen

Graduate Student (Grad Group Immunology)