Peripheral-type benzodiazepine receptor ligands modulate human natural killer cell activity

被引:15
|
作者
Bessler, H
Caspi, B
Gavish, M
Rehavi, M
Hart, J
Weizman, R
机构
[1] Rabin Med Ctr, Hematol & Immunol Res Lab, IL-49372 Petah Tiqwa, Israel
[2] Tel Aviv Univ, Sackler Fac Med, IL-69978 Tel Aviv, Israel
[3] Technion Israel Inst Technol, Fac Med, Dept Pharmacol, Haifa, Israel
[4] Technion Israel Inst Technol, Rappaport Family Inst Res Med Sci, Haifa, Israel
[5] Tel Aviv Univ, Sackler Sch Med, Dept Physiol & Pharmacol, IL-69978 Tel Aviv, Israel
[6] Tel Aviv Community Menatl Hlth Ctr, Tel Aviv, Israel
[7] Tel Aviv Univ, Sackler Fac Med, IL-69978 Tel Aviv, Israel
来源
关键词
natural killer cells; cytotoxicity; peripheral-type benzodiazepine receptor; interleukin-2; interferon;
D O I
10.1016/S0192-0561(97)00013-1
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Following our earlier work, we evaluated the in vitro effect of ligands active at the peripheral-type benzodiazepine receptors on human natural killer cell activity. Peripheral blood mononuclear cells were incubated with benzodiazepine receptor ligands. After 4 h we observed a nonspecific inhibition of natural killer cell activity induced by both peripheral (Ro5-4864 and PK 11195) and central (clonazepam) benzodiazepine receptor ligands; after 24 h, the suppressive activity was specific to peripheral and mixed (diazepam) ligands, and the central-type ligand had no effect. This significant, specific suppression of NK cell activity was completely reversed by the addition of human recombinant interleukin-2 or human leukocyte interferon. Our research provides additional information on the immunomodulatory effects of peripheral-type benzodiazepine ligands. Further studies are needed to clarify the underlying mechanism of natural killer cell inhibition and to determine the clinical implications of these findings. (C) 1997 International Society for Immunopharmacology.
引用
收藏
页码:249 / 254
页数:6
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