Journal
JOURNAL OF NEUROIMMUNOLOGY
Volume 262, Issue 1-2, Pages 46-52Publisher
ELSEVIER
DOI: 10.1016/j.jneuroim.2013.06.006
Keywords
Interleukin 17; Serotonin; 5-HTT; Thymus; Citalopram
Categories
Funding
- Deutsche Forschungsgemeinschaft [Ho 4392/1-1]
- Strategischer Forschungsfonds der Universitat Dusseldorf
- Deutsche Multiple Sklerose Gesellschaft
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Antidepressant drugs, in particular those targeting the serotonin (5-HT)-reuptake system via the serotonin transporter (5-HTT), are known to exhibit antiinflammatory properties and have demonstrated therapeutic efficacy in rodent models of autoimmune disease like experimental autoimmune encephalomyelitis or experimental rheumatoid arthritis. A crucial difference between animal models and the actual human autoimmune disease is the fact that in animals predominantly induced T cells are studied after sensitization with autoantigen. In humans, however, naturally occurring cytokine-producing T cells might play a significant role as well. For this reason, we investigated the effect of the selective serotonin reuptake inhibitor citalopram on cytokine-producing cells in the thymus of C57BL/6 mice, focusing on the (predominantly) T-cell-produced cytokines IL-2, IL-4 and IL-17. Citalopram was able to strongly reduce the frequency of IL-4- and IL-2-producing cells triggered by CD3 stimulation, but exhibited a less pronounced effect on IL-17-producing cells. 5-HTT expression was found to be very low in thymocytes in comparison with splenocytes, and the effect of free extracellular serotonin on CD3-induced thymocyte cytokine production did not mimic the effect of citalopram. We conclude that citalopram has a potent suppressive effect on cytokine production in the thymus, and that this effect is unlikely to be mediated by elevation of extracellular serotonin levels via the 5-HTT. (C) 2013 Published by Elsevier B.V.
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