Introduction:
Recently, particular attention has been paid to research on the inflammatory background of mental disorders. The potential effects of immune cells and cytokines on the development of schizophrenia and affective disorders have been reported. The objective of this article was to familiarize non-psychiatrists with the causes of depressive disorders with a focus on changes in the immune system which cause or exacerbate a major depressive episode. The available literature has been reviewed. Interleukins (IL-1, IL-6) and tumour necrosis factor (TNFα) play the main role in the pathogenesis of mood disorders. The effects of these cytokines lead, directly or indirectly, to the development of unipolar disorder. Stimulation of brain areas associated with mood is believed to be the direct cause, whereas modulation of the hypothalamic-pituitary-adrenal axis (HPA axis) activity or effects on the level of neurotrophins, particularly BDNF, is considered the indirect cause. Inflammatory mediators disrupt the metabolism of tryptophan into serotonin, leading to increased production of kynurenine, which is associated with depressed mood. The relationship between depression and interferon is gaining importance. It is believed that 50% of patients treated with interferon develop depressive symptoms or depression, usually within the first three months of treatment. In conclusion, the relationship between the immune system and depression is evident. One might wonder whether suppression of immune activity might prevent the development of unipolar disorder. Perhaps supplementation with antiinflammatory omega-3 and omega-6 fatty acids might alleviate or even prevent the development of affective symptoms.