The role of 5-HT2B-receptors in fluoxetine-mediated modulation of Th17-and Th1-cells in multiple sclerosis

Fluoxetine is a selective serotonin reuptake inhibitor, which also has an immunomodulatory effect. We investigated the effects of fluoxetine and serotonin (5-HT) on the pro-inflammatory Th17- and Th1-cells in 30 patients with relapsing-remitting MS and 20 healthy subjects. Fluoxetine and 5-HT suppressed IL-17, IFN-gamma and GM-CSF production by stimulated D4(+) T-cells in both groups. Blockade of 5-HT2B-receptors decreased the inhibitory effect of fluoxetine on cytokine production in MS patients. Finally, 5-HT2B-receptor activation inhibits IL-17, IFN gamma and GM-CSF production in both groups. These data suggest an anti-inflammatory role for fluoxetine in MS, which could be mediated by the activation of 5-HT2B-receptors.

Automated summary

Fluoxetine inhibits the production of pro-inflammatory cytokines from Th17 and Th1 cells in both multiple sclerosis patients and healthy subjects by activating 5-HT2B receptors, indicating its potential anti-inflammatory role in MS.