Borysenko M, Borysenko J
Gen Hosp Psychiatry. 1982 Apr;4(1):59-67. doi: 10.1016/0163-8343(82)90028-7.
Research with animal model systems demonstrates a causal relation between stress and disease susceptibility. The physiological sequelae of stressful stimulation vary with type of stressor, chronicity, and perceived control. Different patterns of endocrine secretion are thus associated with specific behavioral parameters. The immune system is regulated at several levels: genetic, cellular, hormonal, and neuronal. Stress and behavioral factors can modulate both cell-mediated and humoral immunity by impacting on the latter three levels of regulation. Both corticosteroids and catecholamines, released as part of the response to aversive stimulation, profoundly inhibit immune responsivity by binding directly to the lymphocyte surface or by releasing secondary mediators that increase the function of suppressor lymphocytes. In addition, there are direct neuroanatomical connections between the hypothalamus and lymphoid organs. Subtle changes in experimental design have yielded significant differences in results that have increased understanding of intermediary mechanisms. Such research complements psychoneuroimmunological and behavioral epidemiological studies in humans.
对动物模型系统的研究表明，压力与疾病易感性之间存在因果关系。应激刺激的生理后遗症因应激源类型、慢性程度和感知控制而异。因此，不同的内分泌分泌模式与特定的行为参数相关。免疫系统在多个层面受到调节：基因、细胞、激素和神经元层面。压力和行为因素可通过影响后三个调节层面来调节细胞介导免疫和体液免疫。作为对厌恶刺激反应的一部分而释放的皮质类固醇和儿茶酚胺，通过直接结合淋巴细胞表面或释放增加抑制性淋巴细胞功能的次级介质，深刻抑制免疫反应性。此外，下丘脑与淋巴器官之间存在直接的神经解剖学联系。实验设计中的细微变化在结果上产生了显著差异，这增进了对中间机制的理解。此类研究对人类心理神经免疫学和行为流行病学研究起到了补充作用。
