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The significance of proinflammatory cytokines and Th1/ Th2 balance in depression and action of antidepressants

Author(s): Teruhisa Komori

In the last 25 years, many reports have indicated that the enhancement of cell-mediated immunity is well recognized in depression, including increased levels of proinflammatory cytokines, which induce sickness behavior. In particular, there has been much interest in the metabolic pathway, from tryptophan to kynurenine. Excessive amounts of proinflammatory cytokines may activate this pathway in depression, resulting in the reduced production of serotonin and increased neurodegenerative products. Neurodegeneration might be involved in the atrophy of several brain regions. However, the reported action of antidepressants on immune function has not been consistent: they have been reported to cause both the suppression and enhancement of proinflammatory cytokines. Furthermore, the effects of antidepressants on the T helper (Th)1/Th2 balance are poorly understood. It is speculated that alterations in the Th1/Th2 balance might result from homeostatic maladjustment in depression, while antidepressants may act as an immunomodulator. What is currently known about proinflammatory cytokines in depression, and the immunomodulatory effects of antidepressant treatments are reviewed.

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