Submitted April 1, 2008
Accepted August 26, 2008
Estrogen inhibits dendritic cell maturation to RNA viruses
Maria M Escribese, Thomas Kraus, Esther Rhee, Ana Fernandez-Sesma, Carolina B Lopez, and Thomas M Moran*
Department of Microbiology, Mount Sinai School of Medicine, New York, NY, United States
Department of Obstetrics, Gynecology and Reproductive Sciences, Mount Sinai School of Medicine, New York, NY, United States
Department of Neurology, Mount Sinai School of Medicine, New York, NY, United States
The Emerging Pathogens Institute, Mount Sinai School of Medicine, New York, NY, United States
The Immunology Institute, Mount Sinai School of Medicine, New York, NY, United States
* Corresponding author; email: thomas.moran{at}mssm.edu.
Dendritic cells (DCs) play a central role in initiating and polarizing the immune response. Therefore, DC maturation represents a key control point in the shift from innate to adaptive immunity. It is suspected that during pregnancy, hormones are critical factors that modulate changes reported to occur in maternal immunity. Here we examined the effect of 17 
-estradiol (E2) on the maturational response triggered by virus in human DCs and its influence on their ability to activate naive T cells. We developed an in vitro system to measure the response of DCs to virus infection with Newcastle disease virus (NDV) following a 24h E2 treatment. Using this system, we demonstrated that E2 pre-treatment down-regulated the anti-viral response to dsRNA viruses in DCs by profoundly suppressing type I interferon (IFN) synthesis and other important inflammatory products. In addition, the DCs capacity to stimulate naive CD4 T cells was also reduced. These results suggest an important role for E2 in suppressing the anti-viral response and provide a mechanism for the reduced immunity to virus infection observed during pregnancy
