Stanford Center on Stress & Health and Department of Psychiatry & Behavioral Sciences, Stanford University, 1201 Welch Road, MSLS Building, P114, Stanford, CA 94305-5485.
Allergy Asthma Clin Immunol. 2008 Mar 15;4(1):2-11. doi: 10.1186/1710-1492-4-1-2.
: It is widely believed that stress suppresses immune function and increases susceptibility to infections and cancer. Paradoxically, stress is also known to exacerbate allergic, autoimmune, and inflammatory diseases. These observations suggest that stress may have bidirectional effects on immune function, being immunosuppressive in some instances and immunoenhancing in others. It has recently been shown that in contrast to chronic stress that suppresses or dysregulates immune function, acute stress can be immunoenhancing. Acute stress enhances dendritic cell, neutrophil, macrophage, and lymphocyte trafficking, maturation, and function and has been shown to augment innate and adaptive immune responses. Acute stress experienced prior to novel antigen exposure enhances innate immunity and memory T-cell formation and results in a significant and long-lasting immunoenhancement. Acute stress experienced during antigen reexposure enhances secondary/adaptive immune responses. Therefore, depending on the conditions of immune activation and the immunizing antigen, acute stress may enhance the acquisition and expression of immunoprotection or immunopathology. In contrast, chronic stress dysregulates innate and adaptive immune responses by changing the type 1-type 2 cytokine balance and suppresses immunity by decreasing leukocyte numbers, trafficking, and function. Chronic stress also increases susceptibility to skin cancer by suppressing type 1 cytokines and protective T cells while increasing suppressor T-cell function. We have suggested that the adaptive purpose of a physiologic stress response may be to promote survival, with stress hormones and neurotransmitters serving as beacons that prepare the immune system for potential challenges (eg, wounding or infection) perceived by the brain (eg, detection of an attacker). However, this system may exacerbate immunopathology if the enhanced immune response is directed against innocuous or self-antigens or dysregulated following prolonged activation, as seen during chronic stress. In view of the ubiquitous nature of stress and its significant effects on immunoprotection and immunopathology, it is important to further elucidate the mechanisms mediating stress-immune interactions and to meaningfully translate findings from bench to bedside.
人们普遍认为，压力会抑制免疫功能，增加感染和癌症的易感性。但矛盾的是，压力也会加剧过敏、自身免疫和炎症性疾病。这些观察结果表明，压力可能对免疫功能产生双向影响，在某些情况下具有免疫抑制作用，而在其他情况下则具有免疫增强作用。最近的研究表明，与抑制或失调免疫功能的慢性压力相反，急性压力可以增强免疫功能。急性压力增强树突状细胞、中性粒细胞、巨噬细胞和淋巴细胞的迁移、成熟和功能，并已被证明可以增强先天和适应性免疫反应。在接触新抗原之前经历急性压力会增强先天免疫和记忆 T 细胞的形成，并导致显著而持久的免疫增强。在再次接触抗原时经历急性压力会增强次级/适应性免疫反应。因此，根据免疫激活和免疫原的情况，急性压力可能会增强免疫保护或免疫病理的获得和表达。相比之下，慢性压力通过改变 1 型细胞因子与 2 型细胞因子的平衡来调节先天和适应性免疫反应，并通过减少白细胞数量、迁移和功能来抑制免疫。慢性压力还通过抑制 1 型细胞因子和保护性 T 细胞，同时增加抑制性 T 细胞功能，增加皮肤癌的易感性。我们曾提出，生理应激反应的适应目的可能是促进生存，应激激素和神经递质充当信号，使免疫系统为大脑感知到的潜在挑战（例如，受伤或感染）做好准备（例如，检测到攻击者）。然而，如果增强的免疫反应针对无害或自身抗原，或者在慢性压力下长期激活后失调，这种系统可能会加剧免疫病理。鉴于压力的普遍存在及其对免疫保护和免疫病理的重大影响，进一步阐明介导应激-免疫相互作用的机制，并将从实验室到临床的研究结果有意义地转化，是非常重要的。
