![]() ![]() 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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