Jennifer Schlezinger, Ph.D.
Associate Professor of Environmental Health
Dr. Schlezinger received her B.S. from Boston College in 1992 and her Ph.D. from the Massachusetts Institute of Technology and Woods Hole Oceanographic Institution Joint Program in Biological Oceanography in 1998. Her PhD research involved the study of the molecular mechanisms of PCB toxicity in a marine fish model. Since coming to Boston University School of Public Health as a post-doctoral researcher in 1998, she has worked closely with Dr. David Sherr on immunotoxicology studies. Dr. Schlezinger is an active member of the Society of Toxiology. Her studies focus on the mechanisms by which environmental contaminants impair the immune system, with particular emphasis on the effects of these contaminants on B cells developing in the bone marrow. Dr. Schlezinger’s studies investigate the role of two receptors, the aryl hydrocarbon receptor (an intracellular protein which is activated by dioxins, polycyclic aromatic hydrocarbons/PAH, and polychlorinated biphenyls/PCBs) and the peroxisome proliferators activated receptor-g (a protein which is activated by endogenous prostaglandins, anti-diabetic drugs, and phthalates), in the death of immature B lymphocytes. New studies in the lab, in collaboration with Dr. Tom Webster, are focusing on the effects of exposure to complex mixtures of environmental contaminants.
Representative Publications:
1. Schlezinger, J. J., D. Liu, M. Farago, D. C. Seldin, K. Belguise, G. E. Sonenshein, D. H. Sherr. 2006. A role for the aryl hydrocarbon receptor in mammary gland tumorigenesis. Biol. Chem. 387(9):1175-87.
2. Schlezinger, J. J., J. K. Emberley, D. H. Sherr. 2006. Activation of multiple MAP kinases in pro/pre-B cells by GW7845, a PPARg agonist, and their contribution to GW7845-induced apoptosis. Toxicol. Sciences. 92(2):433-44.
3. Schlezinger, J. J., W. D. J. Struntz, J. Goldstone, J. J. Stegeman. 2006. Oxidative inactivation of cytochrome P450 1A and production of reactive oxygen species stimulated by halogenated aryl hydrocarbon receptor agonists Aquatic Toxicol. 4 422-432
4. Allan, L. L., J. J. Schlezinger, M. Shansab, D. H. Sherr. 2006. The aryl hydrocarbon receptor (AhR) regulates human primary B lymphocyte growth Biochem. Biophys. Res. Commun. 1 227-235
5. Ryu, H.-Y., J. K. Emberley, J. J. Schlezinger, L.L. Allan, S. Na, D. Sherr. 2005. Environmental chemical-induced bone marrow B cell apoptosis: death receptor-independent activation of a caspase-3 to caspase-8 pathway. Mol. Pharmacol. 4 1087-1096.
6. Schaefer, KL, Denevich, S, Ma, C, Cooley, SR, Nakajima, A, Wada, K, Schlezinger, J, Sherr, D, Saubermann, LJ. 2004. Intestinal antiinflammatory effects of thiazolidenedione peroxisome proliferator-activated receptor-gamma ligands on T helper type 1 chemokine regulation include nontranscriptional control mechanisms. Inflamm. Bowel Dis. 3 244-52
7. Schlezinger, JJ , Howard, G, Hurst, C, Waxman, DJ, Webster, T, Sherr, DH 2004. Environmental and endogenous PPARg agonists induce bone marrow B cell growth arrest and apoptosis: interactions between mono-(2-ethylhexyl) phthalate, 9-cis-retinoic acid, and 15-deoxy-delta12,14-prostaglandin J2. J. Immunol. 5 3165-3177
8. Jensen, BS, Leeman, RJ, Schlezinger, JJ, Sherr, DH 2003. Aryl hydrocarbon receptor agonists suppress interleukin-6 expression by bone marrow stromal cells Environ. Health J. 2 16
9. Allan, LL, Mann, KK, Matulka, RA, Ryu, H-Y, Schlezinger, JJ, Sherr, DH 2003. Bone marrow stromal-B cell interactions in polycyclic aromatic hydrocarbon-induced pro/pre-B cell apoptosis Toxicol. Sci. 2 357
