MECHANISMS OF STRESS-INDUCED MODULATION OF VIRAL PATHOGENESIS AND IMMUNITY

被引:121
作者
DOBBS, CM
VASQUEZ, M
GLASER, R
SHERIDAN, JF
机构
[1] OHIO STATE UNIV,COLL DENT,DEPT ORAL BIOL,COLUMBUS,OH 43210
[2] OHIO STATE UNIV,COLL MED,CTR COMPREHENS CANC,COLUMBUS,OH 43210
关键词
STRESS; HERPES SIMPLEX VIRUS; CYTOTOXIC-T LYMPHOCYTE; RU486; CORICOSTERONE; BETA-ADRENERGIC ANTAGONIST;
D O I
10.1016/0165-5728(93)90187-4
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
A murine model of herpes simplex virus (HSV) infection was used to examine the roles of catecholamines and corticosterone in the restraint stress-induced suppression of viral immunity. Treatment of C57BL/6 mice with RU486, a glucocorticoid receptor antagonist, reversed the stress-induced diminution of cellularity in response to local HSV infection. Treatment of mice with both nadolol, a peripherally acting beta-adrenergic antagonist, and RU486 completely reversed the restraint stress-induced suppression of HSV-specific CTL activation. These findings demonstrate that both corticosterone and catecholamine-mediated mechanisms are operative in the stress-induced suppression of anti-viral cellular immunity.
引用
收藏
页码:151 / 160
页数:10
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