Dhabhar F S
College of Dentistry and College of Medicine, Ohio State University, 4179 Postle Hall, 305 W. 12th. Ave., #192, Columbus, OH 43210-1241, USA.
Ann N Y Acad Sci. 2000;917:876-93. doi: 10.1111/j.1749-6632.2000.tb05454.x.
Delayed-type hypersensitivity (DTH) reactions are antigen-specific, cell-mediated immune responses that, depending on the antigen, mediate beneficial (resistance to viruses, bacteria, fungi) or harmful (allergic dermatitis, autoimmunity) aspects of immunity. Contrary to the widely held notion that stress is immunosuppressive, we have shown that under certain conditions, stress can enhance immune function. DTH reactions can be studied in rats or mice by challenging the pinnae of previously sensitized animals with antigen. Studies have shown that acute stress administered immediately before antigen exposure significantly enhances skin DTH. In contrast, chronic stress significantly suppresses skin DTH. Stress-induced changes in leukocyte distribution may contribute to these bidirectional effects of stress, since acute stress induces a significant mobilization of leukocytes from the blood to the skin, whereas chronic stress suppresses leukocyte mobilization. In order to identify the hormonal mediators of the observed effects of stress, we first showed that adrenalectomy (ADX) eliminates the stress-induced enhancement of DTH. Acute administration (to ADX animals) of low doses of corticosterone and/or epinephrine significantly enhances skin DTH. In contrast, acute administration of high doses of corticosterone, low doses of dexamethasone, or chronic administration of moderate doses of corticosterone, suppress skin DTH. Thus, the timing and duration of stress may significantly affect the nature (enhancing versus suppressive) of the effects of stress on skin immune function. These results suggest that during acute stress, stress hormones may help enhance immune function by informing the immune system about impending challenges (e.g., wounding or infection) that may be imposed by a stressor (e.g., an aggressor). Thus, during acute stress, the brain may send a warning signal to the immune system, just as it does to other fight/flight systems in the body.
迟发型超敏反应（DTH）是抗原特异性的细胞介导免疫反应，根据抗原的不同，介导免疫有益（抵抗病毒、细菌、真菌）或有害（过敏性皮炎、自身免疫）方面。与普遍认为应激具有免疫抑制作用的观点相反，我们已经表明，在某些情况下，应激可以增强免疫功能。可以通过用抗原刺激先前致敏动物的耳廓来在大鼠或小鼠中研究DTH反应。研究表明，在抗原暴露前立即施加急性应激可显著增强皮肤DTH。相反，慢性应激则显著抑制皮肤DTH。应激诱导的白细胞分布变化可能导致应激的这些双向效应，因为急性应激会诱导白细胞从血液大量迁移到皮肤，而慢性应激则抑制白细胞迁移。为了确定应激所观察到的效应的激素介质，我们首先表明肾上腺切除术（ADX）消除了应激诱导的DTH增强。对ADX动物急性给予低剂量的皮质酮和/或肾上腺素可显著增强皮肤DTH。相反，急性给予高剂量的皮质酮、低剂量的地塞米松或慢性给予中等剂量的皮质酮会抑制皮肤DTH。因此，应激的时机和持续时间可能会显著影响应激对皮肤免疫功能影响的性质（增强与抑制）。这些结果表明，在急性应激期间，应激激素可能通过向免疫系统告知应激源（例如攻击者）可能带来的即将到来的挑战（例如受伤或感染）来帮助增强免疫功能。因此，在急性应激期间，大脑可能会向免疫系统发送一个警告信号，就像它对身体中的其他战斗/逃跑系统所做的那样。
