Immunosuppression Following Exposure to Exogenous Estrogens
Abstract
Exposure to pharmacological dosages of estrogens, including 17 beta- estradiol and DES, selectively affects immune responses. This immunologic profile is consistent with myelotoxicity, suppression of cell mediated immunity (CMI), and induction of inflammatory macrophages. Modulation of several of these functions is mediated through the thymus, since thymectomy abolishes estrogen- induced macrophage activation, inhibition of CFU-kinetics and increased susceptibility to Listeria infection, but does not inhibit depression of CMI or bone marrow cellularity. These effects can also be dissociated chemically as zearalanol, an estrogenic mycotoxin, influences macrophage activity and CFU kinetics without affecting CMI. This may be due to structural differences since zearalanol is similar to DES and estradiol in the A-ring region but not D-ring region of the molecule. Underlying this explanation is the demonstration that many of these effects are apparently mediated through estrogen receptors, as indicated indirectly by inhibition with estrogen antagonist and the demonstration of estrogen receptors in thymus and bone marrow cell cytosol preparations.
Document Details
- Document Type
- Technical Report
- Publication Date
- Aug 01, 1983
- Accession Number
- ADP001969
Entities
People
- Gary A. Boorman
- Howard T. Hayes
- Jack H. Dean
- Michael I. Luster
- Oscar Pung
Organizations
- National Institute of Environmental Health Sciences