The possible influence of stress on the immune system, long since suspected by the clinicians in their daily practice, was confirmed by human and animal studies, some of which being recent. Stress generally exert an immunosuppressive effect, but some of its characteristics (nature, duration, intensity, controllability of the stressing situation) can modulate this response, amplifying or reversing it. The concerned mechanisms are complex, involving the autonomic nervous system, the hypothalamo-pituitary complex and its target-glands through hormonal receptors born on immunocompetent cells. The immune system, conversely, is able to inform the brain about the interference of non cognitive stimuli (viruses, bacteria, tumors) through immunologic cell-derived immunohormones active in the central nervous system. Thus, close immune-neuroendocrine interactions exist, in order to cope with stress of all kinds. The stress can act in Graves' disease by depressing the T suppressive function via the hypothalamo-pituitary-adrenal axis, by eliciting the secretion of catecholamines capable of initiating an hyperthyroidism, by facilitating through its immunosuppressive action a viral infection that can have a part in initiating the auto-immune process.