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Stress, depression, the immune system, and cancer.

机译:压力,抑郁,免疫系统和癌症。

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The links between the psychological and physiological features of cancer risk and progression have been studied through psychoneuroimmunology. The persistent activation of the hypothalamic-pituitary-adrenal (HPA) axis in the chronic stress response and in depression probably impairs the immune response and contributes to the development and progression of some types of cancer. Here, we overview the evidence that various cellular and molecular immunological factors are compromised in chronic stress and depression and discuss the clinical implications of these factors in the initiation and progression of cancer. The consecutive stages of the multistep immune reactions are either inhibited or enhanced as a result of previous or parallel stress experiences, depending on the type and intensity of the stressor and on the animal species, strain, sex, or age. In general, both stressors and depression are associated with the decreased cytotoxic T-cell and natural-killer-cell activities that affect processes such as immune surveillance of tumours, and with the events that modulate development and accumulation of somatic mutations and genomic instability. A better understanding of the bidirectional communication between the neuroendocrine and immune systems could contribute to new clinical and treatment strategies.
机译:已经通过心理神经免疫学研究了癌症风险和进展的心理和生理特征之间的联系。下丘脑-垂体-肾上腺(HPA)轴在慢性应激反应和抑郁症中的持续激活可能会损害免疫反应,并有助于某些类型的癌症的发生和发展。在这里,我们概述了各种细胞和分子免疫因素在慢性应激和抑郁中受损的证据,并讨论了这些因素在癌症的发生和发展中的临床意义。由于先前或平行的压力经历,多步免疫反应的连续阶段被抑制或增强,具体取决于压力源的类型和强度以及动物种类,品系,性别或年龄。一般而言,应激源和抑郁都与影响诸如免疫监视肿瘤等过程的细胞毒性T细胞和自然杀伤细胞活性的降低有关,并且与调节体细胞突变的发展和积累以及基因组不稳定性有关。更好地了解神经内分泌和免疫系统之间的双向通讯可能有助于新的临床和治疗策略。

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