Department of Psychiatry & Behavioral Sciences and Stanford Institute for Immunity, Transplantation, & Infection, Stanford University, Stanford, CA 94305-5135, USA.
Integr Comp Biol. 2009 Sep;49(3):215-36. doi: 10.1093/icb/icp045. Epub 2009 Jul 13.
Stress is known to suppress or dysregulate immune function and increase susceptibility to disease. Paradoxically, the short-term fight-or-flight stress response is one of nature's fundamental defense mechanisms that galvanizes the neuroendocrine, cardiovascular, and musculoskeletal systems into action to enable survival. Therefore, it is unlikely that short-term stress would suppress immune function at a time when it may be critically required for survival (e.g., in response to wounding and infection by a predator or aggressor). In fact, studies have shown that stress can enhance immune function under certain conditions. Several factors influence the direction (enhancing versus suppressive) of the effects of stress on immune function: (1) DURATION: acute or short-term stress experienced at the time of activation of an immune response enhances innate and adaptive immune responses. Chronic or long-term stress can suppress or dysregulate immune function. (2) Leukocyte distribution: compartments (e.g., skin), that are enriched with immune cells during acute stress show immuno-enhancement, while those that are depleted of leukocytes (e.g., blood), show immuno-suppression. (3) The differential effects of physiologic versus pharmacologic stress hormones: Endogenous hormones in physiological concentrations can have immuno-enhancing effects. Endogenous hormones at pharmacologic concentrations, and synthetic hormones, are immuno-suppressive. (4) Timing: immuno-enhancement is observed when acute stress is experienced during the early stages of an immune response while immuno-suppression may be observed at late stages. The type of immune response (protective, regulatory/inhibitory, or pathological) that is affected determines whether the effects of stress are ultimately beneficial or harmful for the organism. Arguments based on conservation of energy have been invoked to explain potential adaptive benefits of stress-induced immuno-suppression, but generally do not hold true because most mechanisms for immuno-suppression expend, rather than conserve, energy. We propose that it is important to study, and if possible, to clinically harness, the immuno-enhancing effects of the acute stress response that evolution has finely sculpted as a survival mechanism, just as we study its maladaptive ramifications (chronic stress) that evolution has yet to resolve.
压力会抑制或失调免疫功能，增加患病的易感性。矛盾的是，短期的战斗或逃跑压力反应是大自然的基本防御机制之一，它会使神经内分泌、心血管和肌肉骨骼系统行动起来，以维持生存。因此，在可能需要免疫功能来维持生存的时候（例如，在应对来自捕食者或攻击者的创伤和感染时），短期压力不太可能抑制免疫功能。事实上，研究表明，在某些情况下，压力可以增强免疫功能。有几个因素会影响压力对免疫功能影响的方向（增强或抑制）：
持续时间：在免疫反应激活时经历的急性或短期压力会增强先天和适应性免疫反应。慢性或长期压力会抑制或失调免疫功能。
白细胞分布：在急性压力下富含免疫细胞的隔室（如皮肤）表现出免疫增强，而那些白细胞耗竭的隔室（如血液）则表现出免疫抑制。
生理和药理应激激素的差异效应：生理浓度下的内源性激素具有免疫增强作用。药理浓度下的内源性激素和合成激素具有免疫抑制作用。
时间：在免疫反应的早期阶段经历急性压力时会观察到免疫增强，而在晚期阶段可能会观察到免疫抑制。受影响的免疫反应类型（保护性、调节/抑制性或病理性）决定了压力对机体的影响最终是有益还是有害。基于能量守恒的论点被用来解释应激诱导的免疫抑制的潜在适应性益处，但通常不成立，因为大多数免疫抑制机制会消耗而不是节省能量。我们提出，重要的是研究并在可能的情况下利用急性应激反应的免疫增强效应，因为这种效应是进化作为一种生存机制精心塑造的，就像我们研究其适应不良的后果（慢性应激）一样，而进化尚未解决这个问题。
