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Department of Endocrine, Metabolism and Nephrology, Kochi Medical School, Nankoku 783-8505, Japan

(Requests for offprints should be addressed to T Takao; Email: takaot{at}med.kochi-u.ac.jp)

We determined the effect of 17ß-estradiol on tumor necrosis factor (TNF-)-induced cytotoxicity in human peripheral T lymphocytes (T cells) using lactate dehydrogenase assay. Treatment with 17ß-estradiol (1–100 nM) for 24 h showed dose-dependent reduction of TNF--induced cytotoxicity in T cells. To further evaluate the mechanism of 17ß-estradiol on TNF--induced cytotoxicity in T cells, we identified estrogen receptor (ER) protein in T cells using immunocytochemistry and used the pure ER antagonist ICI 172,780. ER immunoreactivity was clearly observed in T cells. ERß immunoreactivity was also detected in some T cells. ICI 172,780 (10^–7 M) alone did not affect cytotoxicity in T cells, however, ICI 172,780 (10^–7 M) completely abolished 17ß-estradiol cytoprotective effects in T cells. TNF- tended to increase nuclear factor B (NF-B) protein levels in nuclear extracts but it did not reach statistical significance by Western blotting. In contrast, NF-B protein levels in nuclear extracts followed by TNF- with 17ß-estradiol treatment were significantly increased compared with NF-B protein levels in untreated group. NF-B blocker pyrrolidinedithiocarbamate (PDTC) (10^–4 M) alone did not affect cytotoxicity in T cells. In contrast, PDTC (10^–4 M) completely abolished 17ß-estradiol cytoprotective effects in T cells. Caspase -3/-7 activity was significantly increased followed by TNF-, and 17ß-estradiol treatment significantly reduced the increment. The present studies suggest the protective effect of 17ß-estradiol on TNF--induced cytotoxicity through ERs in T cells and that NF-B activation and caspase suppression may be involved in the mechanism.

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