David Sherr, Ph.D.

Environmental Health-School Public Health

Office: 72 E.Concord St R-Bd
Phone: 617-638-6464
Email: dsherr@bu.edu


Recent studies have demonstrated that a number of common environmental carcinogens (i.e. aromatic hydrocarbons, dioxins, PCBs) compromise the immune system as well as induce cancer. These compounds induce thymic atrophy, decrease resistance to infectious agents and transplantable tumors, reduce bone marrow cellularity, alter lymphocyte homing, impair B cell antibody responses, decrease cytotoxic T cell activity, inhibit natural killer activity and decrease cytokine production. Immunotoxicity and carcinogenicity mediated by extremely low concentrations of environmental hydrocarbons is regulated by an intracellular aryl hydrocarbon receptor (AhR). Work from the Sherr laboratory indicates that the AhR is capable of regulating cell growth and death. Consequently, extremely low concentrations of AhR ligands induce programmed cell death (apoptosis) in pre-B cells and in oocytes. Recent studies indicate that the AhR plays a critical role in regulatory T cell and Th17 cell development. Consequently, AhR activation appears to play an important role in regulating inflammatory responses.  Other studies in the Sherr laboratory indicate that AhR hyper-expression and activity characterizes mammary tumor development and probably influences cell growth and tumor invasion through interaction with the promiscuous transcription factor NF-kB and other tumor-associated molecules. Accordingly, current studies in the Sherr lab involve: 1) defining the role of the AhR in inflammation, 2) determining how the AhR contributes to mammary tumorigenesis, and 3) identifying novel AhR inhibitors as potential therapeutics for inflammation and cancer therapy.

Affiliated Websites:

Immunology Training Program Webpage