STRESS-INDUCED MODULATION OF THE PRIMARY CELLULAR IMMUNE-RESPONSE TO HERPES-SIMPLEX VIRUS-INFECTION IS MEDIATED BY BOTH ADRENAL-DEPENDENT AND INDEPENDENT MECHANISMS
STRESS-INDUCED MODULATION OF THE PRIMARY CELLULAR IMMUNE-RESPONSE TO HERPES-SIMPLEX VIRUS-INFECTION IS MEDIATED BY BOTH ADRENAL-DEPENDENT AND INDEPENDENT MECHANISMS
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DOI：
10.1016/0165-5728(93)90007-l
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发表时间：
1993-02-01
影响因子：
3.3
通讯作者：
GLASER, R
中科院分区：
文献类型：
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作者：
BONNEAU, RH;SHERIDAN, JF;GLASER, R
单纯疱疹病毒（HSV）感染的小鼠模型用于检查肾上腺在束缚应激诱导的病毒免疫抑制中的作用。肾上腺依赖性机制对于抑制HSV特异性细胞毒性T淋巴细胞（CTL）的产生是重要的，但对于局部HSV感染相关的淋巴结病的减少并不重要。虽然外源性皮质酮单独给药不能抑制肾上腺切除小鼠的淋巴结病和CTL生成，但束缚应激诱导的肾上腺非依赖性机制与皮质酮协同作用，抑制淋巴结病和CTL发展。这些结果表明，肾上腺依赖性和独立的机制有助于应激诱导的HSV免疫调节。
A murine model of herpes simplex virus (HSV) infection was used to examine the role of the adrenal gland in restraint stress-induced suppression of viral immunity. Adrenal-dependent mechanisms were important for suppressing the generation of HSV-specific cytotoxic T lymphocytes (CTL) but not the associated diminished lymphadenopathy in response to local HSV infection. While exogenous corticosterone administration alone was unable to suppress lymphadenopathy and CTL generation in adrenalectomized mice, an adrenal-independent mechanism induced by restraint stress functioned in synergy with corticosterone to suppress lymphadenopathy and CTL development. These results suggest that both adrenal-dependent and independent mechanisms contribute to stress-induced modulation of HSV immunity.