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Serotonin receptors belong to the G-protein-coupled receptor family with exception of the 5-HT 3 receptor, which is an ion channel ( Barnes and Sharp, 1999). Serotonin operates by activating a family of specific 5-HT receptors, which comprise seven distinct classes based on their structural and functional characteristics. Serotonin (5-hydroxytryptamine, 5-HT) is one of the most extensively studied neurotransmitters in the central nervous system (CNS) regulating multiple physiological functions including the control of anger, aggression, body temperature, appetite, sleep, mood and pain ( Mössner and Lesch, 1998). Our results indicate that there is a crucial role for 5-HT 7R–Cdc42-mediated signaling in the regulation of dendritic cell morphology and motility, suggesting that 5-HT 7R could be a new target for treatment of a variety of inflammatory and immune disorders. Accordingly, migration of dendritic cells in murine colon explants was abolished after pharmacological receptor inhibition. Consistent with this, we observed that 5-HT 7R enhances chemotactic motility of dendritic cells in vitro by modulating their directionality and migration velocity. In addition, basal activity of 5-HT 7R was required for the proper expression of the chemokine receptor CCR7, which is a key factor that controls dendritic cell migration. Although dendritic cell maturation was independent of 5-HT 7R, receptor stimulation affected dendritic cell morphology through Cdc42-mediated signaling.

Here, we demonstrate that expression of serotonin receptor 5-HT7 (5-HT 7R) as well as its downstream effector Cdc42 is upregulated in dendritic cells upon maturation. However, the functional role of serotonin receptors in regulation of dendritic cell functions is poorly understood. Inflammatory processes are often associated with an increased production of serotonin, which operates by activating specific receptors. Dendritic cells are potent antigen-presenting cells endowed with the unique ability to initiate adaptive immune responses upon inflammation.

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