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Psychological stress and immunoprotection versus immunopathology in the skin

机译:心理压力和免疫保护与皮肤免疫病理学的关系

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Stress is thought to suppress immune function and increase susceptibility to infections and cancer. Paradoxically, stress is also known to exacerbate autoimmune/proinflammatory disorders (eg, psoriasis, atopic dermatitis) that should be ameliorated by immunosuppression. Here we review studies showing that although chronic stress (lasting for weeks/months/years) can suppress/dysregulate immune function, acute stress (lasting for minutes to hours) can have immunoenhancing effects. Short-term stress experienced at the time of immune activation enhances dendritic cell, neutrophil, macrophage, and lymphocyte trafficking, maturation, and function, and has been shown to augment innate and adaptive immunity; therefore, depending on the conditions of immune activation, and the nature of the activating antigen, short-term stress can enhance the acquisition and expression of immunoprotection or immunopathology. In contrast, chronic stress suppresses or dysregulates innate and adaptive immune responses by altering the Type 1-Type 2 cytokine balance, inducing low-grade chronic increases in proinflammatory factors, and suppressing numbers, trafficking, and function of immunoprotective cells. Chronic stress also increases susceptibility to skin cancer by suppressing Type 1 cytokines and protective T cells while increasing regulatory/suppressor T cell number/function. It is important to recognize that the adaptive function of a physiological stress response is to promote survival. Stressrelated neurotransmitters, hormones, and factors act as biological alarm signals that prepare the immune and other physiological systems for potential challenges (eg, wounding or infection) perceived by the brain (eg, detection of an attacker); however, this may exacerbate immunopathology (eg, psoriasis, atopic dermatitis) if the enhanced immune response is directed against innocuous or self-antigens, or if the system is chronically activated as seen during long-term 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 both the salubrious and the harmful effects of stress, and to meaningfully translate findings from bench to bedside. ? 2013 Elsevier Inc.
机译:人们认为压力会抑制免疫功能并增加对感染和癌症的敏感性。矛盾的是,还已知压力会加重应通过免疫抑制缓解的自身免疫/促炎性疾病(如牛皮癣,特应性皮炎)。在这里,我们回顾研究表明,尽管慢性应激(持续数周/月/年)可以抑制/调节免疫功能,但急性应激(持续数分钟至数小时)可以具有免疫增强作用。免疫激活时经历的短期应激会增强树突状细胞,嗜中性粒细胞,巨噬细胞以及淋巴细胞的运输,成熟和功能,并已显示出增强先天和适应性免疫的能力。因此,根据免疫激活的条件和激活抗原的性质,短期应激可以增强免疫保护或免疫病理学的获得和表达。相反,慢性应激通过改变1-型2型细胞因子平衡,诱导促炎因子的低度慢性增加以及抑制免疫保护细胞的数量,运输和功能来抑制或失调先天和适应性免疫应答。慢性应激还可以通过抑制1型细胞因子和保护性T细胞,同时增加调节性/抑制性T细胞的数量/功能来增加对皮肤癌的敏感性。重要的是要认识到,生理应激反应的适应功能是促进生存。与压力有关的神经递质,激素和因子可作为生物警报信号,为免疫和其他生理系统做好准备,以应对大脑感知到的潜在挑战(例如,受伤或感染)(例如,检测攻击者);但是,如果增强的免疫反应针对无害或自身抗原,或者如长期应激所见,该系统被长期激活,则可能会加剧免疫病理(例如牛皮癣,特应性皮炎)。考虑到压力的普遍性及其对免疫保护和免疫病理学的显着影响,重要的是进一步阐明介导压力的有害作用和有害作用的机制,并将发现结果从实验台有效地转化为床旁。 ? 2013爱思唯尔公司

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