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