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All Investigators
Bonnie N. Dittel, PhD

Bonnie N. Dittel, PhD

Senior Investigator

Adjunct Faculty
Department of Microbiology and Molecular Genetics
Medical College of Wisconsin

Education and Training

Postdoctoral Training
Yale University

Doctoral Training
University of Minnesota, Ph.D., 1994

Contact Us

Bonnie N. Dittel, PhD

Senior Investigator
(414) 937-3865 Fax: (414) 937-6284

  • Research Interests


    The focus of our research program is to investigate cellular and molecular mechanisms involved in the regulation of inflammation. Inflammation is a component of virtually every disease and if not controlled can lead to severe tissue damage. The primary disease model utilized in the laboratory is the mouse model of multiple sclerosis (MS), experimental autoimmune encephalomyelitis (EAE). MS is an autoimmune disorder of the central nervous system (CNS) and is characterized by focal areas of inflammation. In past studies, we have extensively utilized EAE to study negative immune regulatory mechanisms that keep inflammation in check within the CNS. Our current studies have expanded to mouse models of contact dermatitis (contact hypersensitivity) and inflammatory bowel disease (DSS-colitis). 

    Current Research Interests

    Regulatory B cells (Breg)

    B cell regulation of autoimmunity was first demonstrated in the EAE model, whereby mice deficient in B cells were unable to recover from the clinical signs of EAE. In our studies, we have found that B cells regulate the severity of EAE by interactions with Foxp3+ T regulatory cells (Treg) in a GITRL-dependent manner. Specifically, we found that B cells play an essential role in Treg homeostasis whereby they maintain Treg numbers at a sufficient level to dampen inflammation. Current studies are investigating the development, phenotype and localization of this novel subset of regulatory B cells. These studies utilize the EAE and contact hypersensitivity models. The goal of this research is to undercover a novel Breg subset that can be exploited for cell-based therapies for the treatment of inflammatory disorders.

    Myeloperoxidase (MPO)

    MPO is a myeloid-lineage restricted enzyme that utilizes H2O2 to generate hypochlorous acid that has strong antibacterial properties. In sterile inflammation, such as MS, MPO and MPO-derived oxidants are thought to be pathogenic promoting inflammation and causing tissue damage. In particular, MPO has been implicated in vascular permeability. In MS, the opening of the blood-brain barrier (BBB) is considered detrimental. The presence of MPO within inflammatory lesions in MS patients along with our studies in the EAE model, suggests that it plays a pathogenic role in MS. Using a novel inhibitor of MPO, we have found that its inhibition during EAE rapidly attenuates disease severity that is associated with sealing of the BBB. Current studies in the lab are focused on the pathogenic role of MPO in inflammation with an emphasis on vascular permeability. In addition to EAE, these studies also utilize the contact hypersensitivity and DSS-colitis models in which permeability is also considered pathogenic. The goal of this research is to undercover the mechanism whereby MPO induces vascular and epithelial permeability and to determine whether MPO is a viable therapeutic target for the treatment of inflammatory diseases.


    It is now clear that interactions between the immune system and microbiome have consequences for human health. In past studies, we utilized microbiome analysis to study microbial dysbiosis in the gut in IL-10-deficient mice. In current studies, we are utilizing this knowledge and expertise to determine how

  • Grant Support
    • 1R56AI122655 - 01A1, NIAID, Mechanisms of a novel regulatory B cell subset  
    • 1R56AI129348-01A1, NIAID, B cell-mediated immune regulation
    • Teva Investigator Sponsored Studies, Teva Pharmaceuticals, Access the ability of Copaxone to enhance the regulatory activity of a novel B cell subset
    • RG 1501-03034, National Multiple Sclerosis Society, Characterization of a Novel Regulatory B Cell Subset that Attenuates EAE
    • Medical College of Wisconsin, Cancer Center pilot grant, Can chronic lymphocytic leukemia (CLL) exhibit regulatory B cell function?
  • Lab

    Hong Mei
    Research Technologist

    Cody Gurski
    Research Technologist

    Mohamed Khalil
    Research Scientist I  

  • Publications

    Regulatory B cells

    • Mann, M.K., K. Maresz, L.P. Shriver, T. Tan, and B.N. Dittel. 2007. B cell regulation of CD4+CD25+ T regulatory cells and IL-10 via B7 is essential for recovery from experimental autoimmune encephalomyelitis. J. Immunol. 178:3447-3456.
    • Ray, A., S. Basu, C. Williams, N. Salzman and B.N. Dittel. 2012. A novel IL-10-independent regulatory role For B cells in suppressing autoimmunity by maintenance of regulatory T cells via GITRL. J. Immunol. 188:3188-3198.
    • Mann, M.K., A. Ray, S. Basu, C. Karp and B.N. Dittel. 2012. Pathogenic and regulatory roles for B cells in experimental autoimmune encephalomyelitis. Autoimmun. 45:388-399. Wang, L., A. Ray, X. Jiang, J-Y. Wang, S. Basu, X. Liu, T. Qian, B.N. Dittel and Y. Chu. 2015. T regulatory cells and B cells cooperate to form a regulatory loop that maintains gut homeostasis and suppresses dextran sulfate sodium-induced colitis. Mucosal Immunol. 8:1297-1312.
    • Ray, A and B.N. Dittel. 2017. Mechanisms of regulatory B cell function in autoimmune and inflammatory diseases beyond IL-10. J. Clin. Med. 6, 12; doi:10.3390/jcm6010012


    • Zhang, H., A. Ray, N.M. Miller, D. Hartwig, K.A. Pritchard, Jr., and B.N. Dittel. 2015. Inhibition of myeloperoxidase at the peak of experimental autoimmune encephalomyelitis restores blood-brain-barrier integrity and ameliorates disease severity. J. Neurochem. 136:826-836.
    • Strzepa, A, K.A. Pritchard and B.N. Dittel. 2017 Myeloperoxidase: A new player in autoimmunity. Cell. Immunol. 317:1-8.


    • Ray, A., S. Basu, R.Z. Gharaibeh, L.C. Cook, R. Kumar, E.J. Lefkowitz, C.R. Walker, C.D. Morrow, C.L. Franklin, T.L. Geiger, N.H. Salzman, A.F. Fodor and B.N. Dittel. 2015. Gut microbioal dysbiosis due to Helicobacter drives and increase in marginal zone B cell in the absence of IL-10 signaling in macrophages. J. Immunol. 195:3071-3085.
    • Ray, A. and B.N. Dittel. 2015. Interrrelatedness between dysbiosis in the gut microbiota due to immunodeficiency and disease penetrance of colitis. Immunol. 146:359-368.

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