Eva Tsuda MD
|Institution||University of Massachusetts Medical School|
|Address||University of Massachusetts Medical School|
55 Lake Avenue North
Worcester MA 01655
|Institution||UMMS - School of Medicine|
|Institution||UMMS - Graduate School of Biomedical Sciences|
|Department||Immunology and Virology|
|Institution||UMMS - Programs, Centers and Institutes|
|Department||Center for AIDS Research|
MD, Semmelweis Medical School, Budapest, Hungary
Interactions of viral gene products and host immune systems
I have started my career in molecular virology, and worked on a variety of DNA tumor viruses. Later, in the 1990s I have changed the focus of my work, concentrating on viral immunology and pathogenesis. The main goal of my studies in a broad sense is to understand how viral gene products and components of the host immune system (innate and adaptive) interact and contribute to control virus infections, and virus-induced tumors. For many years I have been studying the immunological control of murine polyomavirus (PyV) in mice, a natural host-virus model. Our report on T cell-independent IgG responses to PyV was the first to show that a virus infection can generate protective IgG to antigens which are chemically proteins, in the absence of T cells. More recently, we published the important observation that MyD88-mediated pathways are required for long-term antibody responses to PyV, as MyD88 knock-out (KO) mice have decreased serum IgG responses, greatly reduced long-lived plasma cell population in the bone marrow, and diminished memory B cell responses compared to wild type mice. These data suggest an essential role for the MyD88-mediated pathways in the generation of long-term humoral immunity. Presently our efforts are aimed to elucidate the signals/pathways in B cells, follicular helper T cells (TFH) and accessory cells that are essential for the generation and maintenance of life- long humoral immunity and the molecular mechanisms involved in these processes.
Potential Rotation Projects Include
- Characterization of innate receptor activation by PyV on various cell types
- Determining what steps of B cell responses are affected in PyV-infected mice with MyD88 mutationn in B cells or other cell types.
- Testing signals (surface and soluble) that regulate TI IgG isotype switching in T cell-deficient PyV-infected mice
- Testing the immunological basis of susceptibility to PyV-induced tumors: role of NK and gd T cells
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