General Research InterestStudies 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 DescriptionDr. 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 WorkCollaboration with Dr. John Byrd on how CD86 signaling in a B cell may affect the level of the antibody response to the pneumonia vaccine.