Neuromediators may modulate neuroinflammation, particularly in multiple sclerosis (MS). We investigated the effects of dopamine (DA) on the pro-inflammatory Th17-branch of immunity in 43 patients with relapsing-remitting MS and 20 healthy subjects. Serum DA was lower in MS relapse, whereas percentages of blood CD4(+)CD26(+)CD161(+)CD196(+) Th17-cells and production of interleukin-17 (IL-17) and interferon-gamma by anti-CD3/anti-CD28-stimulated peripheral blood mononuclear cells (PBMC) were higher in MS relapse than in remission or healthy subjects. DA suppressed IL-17 production by PBMC from MS patients and healthy subjects. The suppressive effect of DA was abolished in the presence of an antagonist of D2-like receptors (sulpiride). These data suggest an anti-inflammatory role for DA in MS.