Faculty

 Margaret Bynoe

Assistant Professor of Immunology Cornell University College of Veterinary Medicine C5 149 Veterinary Medical Center E-mail: msb76@cornell.edu Phone: 607-253-4023 PhD (Albert Einstein College of Medicine)

Dr. Margaret Bynoe, an Assistant Professor in the Department of Microbiology and Immunology, received her Bachelor of Science in Biology from the Long Island University and her PhD from the Albert Einstein College of Medicine. She received her postdoctoral training and became an Associate Research Scientist at Yale University School of Medicine.

 Research Interests / Lab Members / Related Links / Selected References

Research Interests

My research interests focuses on models of antigen-specific immune responses that can lead to immune suppression against autoimmune diseases (such as experimental allergic encephalomyelitis (EAE), the mouse model for the human disease multiple sclerosis) or induction of effector immune responses that can elicit immunity against tumors. The utility of non-invasive antigen delivery system is at the core of these studies. We previously employed the epicutaneous or transdermal delivery of self-antigen in transgenic mice with most T cells expressing a T cell receptor (TCR) specific for the N-terminal peptide (Ac1-11) of myelin basic protein (MBP TCR Tg mice). In this approach, Ac1-11 loaded on an adhesive patch is applied to the shaved skin of mice for two weeks prior to disease induction by conventional procedure (Ac1-11 in CFA). We observed significant protection from both spontaneous and immunization-induced forms of EAE (Bynoe et al., 2003). Protection was antigen specific since the epicutaneous application of control antigens, other than Ac1-11 (namely myelin oligodendrocyte glycoprotein (MOG)35-55 and proteolipid protein (PLP)139-151) did not confer protection against disease. In addition, ECi could be used to protect other mouse strains from relapsing-remitting EAE. The protection observed in MBP TCR Tg mice epicutaneously treated with Ac1-11 alone was mediated by antigen-specific CD4 T cells that were able to transfer resistance to unmanipulated syngeneic recipients. These induced CD4 suppressor T (Ts) cells were able to inhibit, in a cell-cell contact dependent fashion, the specific proliferative response and IFN-? secretion of their naïve counterparts in vitro. ECi-induced Ts cells remained consistently CD25-, and did not produce Th2 or Th3 response-associated major cytokines such as IL-4, IL-10, IL-13 or TGF-? upon stimulation.

Ongoing and future work in the lab addresses 1) the mechanism of antigen-specific T suppressor cell induction by epicutaneous immunization, 2) the molecular mechanism of how T suppressor and or T regulatory cells suppress effector T cell function, 3) the utility of epicutaneous immunization in the development of immunity against cancer. From these questions, we hope to gain insight into how the mature immune system can be re-educated or re-directed to avert autoimmunity while still enabling normal immune effector function to prevail.

Graduate Fields

Dr. Bynoe is a member of the following Graduate Fields:

Compartive Biomedical Sciences
Immunology

 

Lab Members

Jeff Mills, Postdoctoral Associate
Cindy Mueller, Technial Support

Program in Infection & Pathobiology

Bynoe MS. 2004. Epidermal Antigen Presenting Cells are Tolerogenic Under Conditions of Skin Immunizattion with Self-peptide. Immunology International Proceedings, MEDIMOND. Volume ISBN 88-7587-069-1.

Bynoe MS, Evans JT, Viret C, Janeway CA Jr. 2003. Epicutaneous immunization with autoantigenic peptides induces T suppressor cells that prevent experimental allergic encephalomyelitis. Immunity 19:317-328.

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Last Revised on February 20, 2007

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