Modulation of HLA-DR Expression in Epithelial Cells by Interleukin 1 and Estradiol-17β*

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Abstract
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. Lipopolysaccharides, 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 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.