Principal investigator: Richard J. Levine, M.D., M.P.H., M.S.
Recent studies have revealed the frequent presence of bidirectional cell traffic between mother and fetus. Dr. Levine is interested in the possible role of circulating fetal cells or cellular fragments in causing preeclampsia, perhaps by initiating an inflammatory response which damages endothelial cells. Cells of maternal origin can also enter and persist in the offspring and may be linked to the development of inflammatory and/or autoimmune disorders in children and adults. A pilot study is underway to investigate the potential for maternal microchimerism to contribute to the pathogenesis of type 1 diabetes.
DESPR Collaborators
· Kai F. Yu, Ph.D.
· James L. Mills, M.D., M.S.
Selected Publications
Levine RJ, Qian C, LeShane ES, Yu KF, England LJ, Schisterman EF, Wataganara T, Romero R, & Bianchi DW. (2004). Two-stage elevation of cell-free fetal DNA in maternal sera before onset of preeclampsia. Am J Obstet Gynecol, 190:707-713. [Abstract]
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