Shannon Z. Jones
936 Mary Ellen Jones Bldg, CB# 7365
Chapel Hill, NC 27599
Tel: (919) 966-0916
Fax: (919) 966-5640
Education
Doctorate of Philosophy
Curriculum in Toxicology
Research Advisor: Dr. Lee M. Graves
Date of Matriculation: June 2006
Bachelor of Science in Molecular Biology
Department of Life Sciences
Winston-Salem State University, Winston-Salem, NC, May 2006
Awards
2007 Recipient of Society of Toxicology (SOT) Travel Award
2007-2008 Howard Hughes Medical Institute Med into Grad UNC Program in Translation Medicine Fellowship Recipient
Dissertation
“The Application of Novel Antibody Microarrays to Characterize CD Antigen Expression in Systemic Lupus Erythematosus.”
Advisor: Dr. Lee M. Graves
Systemic Lupus Erythematosus (SLE) is an autoimmune disease characterized by the production of autoantibodies against nuclear antigens, and is most commonly diagnosed in women. The cause of lupus is currently unknown, but there are environmental and genetic factors involved. Some environmental factors, which may trigger the disease, include infections, antibiotics, ultraviolet light, extreme stress, certain drugs, and hormones. The development of autoimmunity in SLE is a process that is believed to involve both T and B cells. Cluster of Differentiation (CD) antigens are cell surface proteins that define the properties of T and B cells. While some changes in CD antigen expression of these cells in SLE have already been characterized, the large-scale analysis of CD antigen expression in patients with SLE has not been examined. The MedsaicTMAntibody Microarray System is a breakthrough technology that simultaneously measures the expression of up to 150 CD antigens. The value of this approach is that it offers an unbiased, comprehensive analysis of CD antigens expression in normal and diseased cells. The detailed knowledge of CD antigen expression provides an important “fingerprint” of normal and diseased states, including SLE. The goal of my project is to identify changes in CD antigen expression that are characteristic of SLE and identify unique “biomarkers” of this disease. To accomplish this, we studied the MRL/lpr mouse strain, a prominent and well-characterized animal model of lupus. Specifically, we compared CD antigen expression of isolated splenocytes from normal C57Bl6 mice and MRL/lpr lupus prone mice. Our results show that the expression of CD11a and CD44 were upregulated in the MRL/lpr mouse. Both CD11a and CD44 have been previously shown to be upregulated in human lupus. Further studies, using the MRL/lpr mouse strain, have also shown the down-regulation of CD31. Previous reports have suggested that CD31 may play an important role in the development of SLE. Taken together, these results demonstrate the validity of this antibody microarray system, and suggest that it will be a useful tool in identifying CD antigen molecules that are involved in the pathogenesis of SLE. Future studies will involve the characterization of CD antigen expression in human SLE, to further identify potential biomarkers of this disease. My project will also involve analysis of the effects of HSP90 inhibition on CD antigen expression, and its evaluation as a potential treatment for SLE, since HSP90 is known to upregulated in human lupus.
Personal Interests
I enjoy reading, traveling, and most importantly, spending time with my family, friends, and loved ones.