Dopamine Receptor D5 Signaling Plays a Dual Role in Experimental Autoimmune Encephalomyelitis Potentiating Th17-Mediated Immunity and Favoring Suppressive Activity of Regulatory T-Cells.

ABSTRACT: A number of studies have shown pharmacologic evidence indicating that stimulation of type I dopamine receptor (DR), favors T-helper-17 (Th17)-mediated immunity involved in experimental autoimmune encephalomyelitis (EAE) and in some other inflammatory disorders. Nevertheless, the lack of drugs that might discriminate between DRD1 and DRD5 has made the pharmacological distinction between the two receptors difficult. We have previously shown genetic evidence demonstrating a relevant role of DRD5-signaling in dendritic cells (DCs) favoring the CD4⁺ T-cell-driven inflammation in EAE. However, the role of DRD5-signaling confined to CD4⁺ T-cells in the development of EAE is still unknown. Here, we analyzed the functional role of DRD5-signaling in CD4⁺ T-cell-media

SUBMITTER: Osorio-Barrios F 

PROVIDER: S-EPMC6048279 | biostudies-literature | 2018

REPOSITORIES: biostudies-literature