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ToxSci Advance Access published online on May 27, 2004
Toxicological Sciences, doi:10.1093/toxsci/kfh179
Toxicological Sciences © Society of Toxicology 2004; all rights reserved
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Received March 19, 2004
Accepted May 18, 2004

Immunotoxiocology

Endocrine Disruptors (Environmental Estrogens) Enhance Autoantibody Production by B1 Cells

Hideaki Yurino 1, Sho Ishikawa 1, Taku Sato 1, Kenji Akadegawa 1, Toshihiro Ito 1, Satoshi Ueha 1, Hidekuni Inadera 2, Kouji Matsushima 1*

1 Department of Molecular Preventive Medicine, School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-0033, Japan
2 Department of Public Health, Toyama Medical and Pharmaceutical University, 2630 Sugitani, Toyama, 930-0194, Japan

* To whom correspondence should be addressed. E-mail: koujim{at}m.u-tokyo.ac.jp.


  Abstract

Accumulating data suggest that endocrine disruptors affect not only the reproductive system, but also the immune system. We demonstrate here that endocrine disruptors including diethylstilbestrol (DES) and bisphenol-A (BPA) enhance autoantibody production by B1 cells both in vitro and in vivo. BWF1 mice, a murine model for SLE, implanted with silastic tubes containing DES after orchidectomy developed murine lupus characterized by IgG anti-DNA antibody production and IgG deposition in the glomeruli in the kidney as well as those implanted with 17{beta}-estradiol (E2). Plaque forming cells (PFC) producing autoantibodies specific for bromelain-treated RBC were significantly increased in mice implanted with DES and BPA. IgM antibody production by B1 cells in vitro was also enhanced in the presence of endocrine disruptors including DES and BPA. Estrogen receptor (ER) expression was up-regulated in B1 cells in aged BWF1 mice developing lupus nephritis. These results suggest that endocrine disruptors are involved in autoantibody production by B1 cells and can be a possible etiologic factor in the development of autoimmune diseases.

Key Words: endocrine disruptors, environmental estrogens, autoantibody, B cell, SLE .


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