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Journal of Clinical Endocrinology & Metabolism, Vol 71, 740-747, Copyright © 1990 by Endocrine Society
ARTICLES |
SS Tabibzadeh, A Sivarajah, D Carpenter, BM Ohlsson-Wilhelm and PG Satyaswaroop
Department of Pathology, City Hospital Center, Elmhurst, New York 11373.
Both ultrapure human interleukin-1 (IL-1) and Escherichia coli derived recombinant IL-1 alpha and beta consistently induced the expression of major histocompatibility class II (HLA-DR) molecules in a human endometrial and a breast carcinoma cell line. [35S]Methionine incorporation into IL-1 induced, immunoprecipitable HLA-DR molecules demonstrated de novo synthesis of both light and heavy chains of the HLA-DR molecules. Lipopolysaccharide, recombinant interleukin-2 and recombinant interleukin-6 failed to induce HLA-DR expression in these epithelial cells. In contrast to the dramatic effect on HLA-DR expression, IL-1 had no effect on the epithelial cell proliferation. Pretreatment of T47D cells with estradiol-17 beta significantly decreased the IL-1 induced HLA-DR expression, and pretreatment of IL-1 with an IL-1 specific antibody, neutralized IL-1 action. These studies demonstrate that a cytokine (IL-1) and a sex steroid hormone estradiol- 17 beta can interact to regulate the expression of HLA-DR molecules in epithelial cells.
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