Dantzer R, Kelley K W
INRA-INSERM, U 259, Bordeaux, France.
Life Sci. 1989;44(26):1995-2008. doi: 10.1016/0024-3205(89)90345-7.
The old notion that stress exacerbates the progression of physical illness via its corticosteroid-mediated immunosuppressive effects must be revised. Experimental and clinical studies demonstrate that both laboratory and natural stressors alter the activities of lymphocytes and macrophages in a complex way that depends on the type of immune response, the physical and psychological characteristics of the stressor and the timing of stress relative to the induction and expression of the immune event. The influences of stress on immunity are mediated not only by glucocorticoids but also by catecholamines, endogenous opioids and pituitary hormones such as growth hormone. Sensitivity of the immune system to stress is not simply fortuitous but is an indirect consequence of the regulatory reciprocal influences that exist between the immune system and the central nervous system. The immune system receives signals from the brain and the neuroendocrine system via the autonomic nervous system and hormones and sends information to the brain via cytokines. These connections appear to be part of a long-loop regulatory feedback system that plays an important role in the coordination of behavioral and physiological responses to infection and inflammation.
应激通过其皮质类固醇介导的免疫抑制作用加剧身体疾病进展这一旧观念必须修正。实验和临床研究表明，实验室应激源和自然应激源均以复杂方式改变淋巴细胞和巨噬细胞的活性，这取决于免疫反应类型、应激源的生理和心理特征以及应激相对于免疫事件诱导和表达的时间。应激对免疫的影响不仅由糖皮质激素介导，还由儿茶酚胺、内源性阿片类物质和垂体激素（如生长激素）介导。免疫系统对应激的敏感性并非偶然，而是免疫系统与中枢神经系统之间存在的调节性相互影响的间接结果。免疫系统通过自主神经系统和激素接收来自大脑和神经内分泌系统的信号，并通过细胞因子向大脑发送信息。这些联系似乎是长环调节反馈系统的一部分，该系统在协调对感染和炎症的行为及生理反应中起重要作用。
