The cigarette tar component p-benzoquinone blocks T-lymphocyte activation by inhibiting interleukin-2 production, but not CD25, ICAM-1, or LFA-1 expression

被引:23
作者
Geiselhart, LA
Christian, T
Minnear, F
Freed, BM
机构
[1] ALBANY MED COLL, TRANSPLANTAT IMMUNOL & HISTOCOMPATIBIL LAB, ALBANY, NY 12208 USA
[2] ALBANY MED COLL, CELLULAR IMMUNOL & FLOW CYTOMETRY LAB, ALBANY, NY 12208 USA
[3] ALBANY MED COLL, DEPT PHYSIOL & CELL BIOL, ALBANY, NY 12208 USA
[4] ALBANY MED COLL, DEPT SURG, ALBANY, NY 12208 USA
关键词
D O I
10.1006/taap.1996.8071
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Cigarette smoking has been shown to cause profound suppression of T-cell responses in the lungs, but the mechanism by which this phenomenon occurs is not known. We have shown that 10 mu M p-benzoquinone (p-BQ), a thiol-reactive benzene derivative found in cigarette tar, inhibits mitogen-induced IL-2 production by human peripheral blood mononuclear cells by 76 +/- 7% without affecting lymphocyte/macrophage agglutination or blast transformation. The effect of p-BQ appeared to be specific for IL-2 production, since de novo induction of the IL-2 receptor alpha-chain (CD25) and ICAM-1 (CD54) and upregulation of LFA-1 alpha/beta (CD11a and CD18) were unaffected. In contrast, N-ethylmaleimide (NEM), another alpha,beta-unsaturated diketone with thiol-reactive properties similar to those of p-BQ, inhibited all of these Con A-induced activation events. These results suggest that p-BQ inhibits T-cell mitogenesis by blocking a thiol-dependent event that controls IL-2 production but not other T-cell activation events. (C) 1997 Academic Press.
引用
收藏
页码:30 / 36
页数:7
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