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Cytokines, which appear to be altered in some depressed patients, have been hypothesized to be involved in the pathogenesis of depression. Nevertheless, numerous methodological problems need to be solved before this hypothesis can be confirmed. In animals, the role of cytokines in the activation of both the HPA axis and brain metabolism has only been demonstrated in acute situations, whereas chronic experiments should be more appropiate to reproduce a depression-like situation. Furthermore, cytokines act as a complex network that has to be studied in more details in depression.

If cytokines play a role in the pathphysiology of depression, antidepressants should be active on cytokine production and/or action. However, there is no evidence so far to conclude whether depressed mood is associated with severity of illness or whether it is directly linked to the cytokine concentrations measured in these patients. The comparison of the efficacy of antidepressant drugs with alternative therapies (e.g. electroconvulsive therapy or psychotherapy) should help to answer this question. Furthermore, depending on their molecular heterogeneity, antidepressants could have different effects on cytokine production, and a systematic study of the effects of different classes of antidepressants needs to be carefully done. Last, but not the least, if cytokines are involved in the pathogenesis of depression, molecules known to modulate the inflammatory cytokine production, like receptor-antagonists, anti-cytokine antibodies, or anti-inflammatory cytokines, should improve depressive disorders.

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