Virginia Sanders M PhD

Virginia Sanders M PhD
ProfessorCollege of Medicinesanders.302@osu.edu
319 Behavioral Med Research, Inst 460 Medical Center Drive Columbus Ohio 43210
Phone:614-685-6749Fax: (614) 292-9805
  • Non-Member

General Research Interest

Studies the ability of the sympathetic nervous system to mediate important changes in adaptive immunity via the neurotransmitter norepinephrine and stimulation of the beta2-adrenergic receptor on T and B lymphocytes.

Research Description

Dr. Sanders is a Professor, in the Dept. of Molecular Virology, Immunology, & Medical Genetics and the Director of the Integrated Biomedical Science Graduate Program in the College of Medicine. Dr. Sanders' research has focused on the ability of the nervous system to mediate important changes in adaptive immunity via the neurotransmitter norepinephrine and stimulation of the beta2-adrenergic receptor on T and B lymphocytes. She has shown that the stimulation of this neurotransmitter receptor on a B cell upregulates B cell costimulatory molecule (CD86; also known as B7-2) expression and direct signaling (J. Immunology, 1997, 1999, 2000, 2001, 2002, 2003, 2006, 2007; J. Biol. Chem., 2004). Her research now focuses on understanding the mechanism by which CD86 stimulation activates a direct signaling pathway within a primary or transformed B cell either before or after exposure to norepinephrine.  With this knowledge, she plans to study the mechanism by which CD86-induced signals delivered directly to a transformed cell regulate cell growth and differentiation.  Such an approach is unique since the ability of CD86 to signal directly has only recently been recognized, offering an alternative means of regulation that may synergize with the well-known role of CD86 in regulating a T cell response against a transformed cell.  Furthermore, these immune- and neuro-receptor-induced immune alterations appear to play an important role in the response of B cells to a vaccine for pneumonia, which is one of the leading causes of death in cancer patients. Dr. Sanders has established a recent collaboration with Dr. John Byrd to pursue the latter studies. The second research project involves a study of the regulation of the IgE response by norepinephrine and stimulation of the beta2-adrenergic receptor on a B cell.  The data show that the link between the beta2-adrenergic receptor activation of PKA and the increase measured in p38 MAPK involves the PKA-dependent activation of hematopoietin protein tyrosine phosphatase that causes the release of bound p38 MAPK, making it available for phosphorylation via the CD40-actiavted MAPK pathway Cell Mol Biol 2008).  This phosphatase may serve as a target for allergy co-therapy so that the B cell response will be unaffected by a beta2-adrenergic agonist, but the desired bronchodilation effect would be maintained. Dr. Sanders is an experienced laboratory-based mentor and has trained dozens of doctoral and post-doctoral students.

Transinstitutional Work

Collaboration with Dr. John Byrd on how CD86 signaling in a B cell may affect the level of the antibody response to the pneumonia vaccine.

Current Publications

  • Padro CJ, Shawler TM, Gormley MG, Sanders VMAdrenergic regulation of IgE involves modulation of CD23 and ADAM10 expression on exosomes.J Immunol 191 5383-97 12/1/2013
  • Lucas CR, Cordero-Nieves HM, Erbe RS, McAlees JW, Bhatia S, Hodes RJ, Campbell KS, Sanders VMProhibitins and the cytoplasmic domain of CD86 cooperate to mediate CD86 signaling in B lymphocytes.J Immunol 190 723-36 1/15/2013
  • Xin J, Mesnard NA, Beahrs T, Wainwright DA, Serpe CJ, Alexander TD, Sanders VM, Jones KJCD4+ T cell-mediated neuroprotection is independent of T cell-derived BDNF in a mouse facial nerve axotomy model.Brain Behav Immun 26 886-90 8/1/2012

The Ohio State University Comprehensive Cancer Center – Arthur G. James Cancer Hospital and Richard J. Solove Research Institute (OSUCCC – James) 300 W. 10th Ave. Columbus, OH 43210 Phone: 1-800-293-5066 | Email: jamesline@osumc.edu