Contributions
Abstract: P426
Type: Poster
Abstract Category: Pathology and pathogenesis of MS - Immunology
Introduction: Multiple sclerosis (MS) - chronic autoimmune disease of the CNS predominantly mediated by T-cells. Dopamine (DA) can participate in MS pathogenesis modulating immune cells activity and cytokine production.
Objective: To study the relationship between clinical impairment, DA concentration in the serum, quantitative characteristics of Тh17-cells, and to clarify the influence of DA on the function of Th17 cells.
Materials and methods: Data from 43 patients with relapsing-remitting MS and 20 healthy controls were included. Fourteen patients were examined during relapses, 29 during clinical remission. The DA concentration in the serum was measured by ELISA. Circulating Th17-cells were determined by flow cytometry (CD4+CD26+CD161+CD196+). The levels of interleukin-17 (IL-17) and interferon-gamma (IFN-γ) were studied by ELISA in supernatants of peripheral blood mononuclear cells (PBMC) stimulated with microbeads coated with anti-CD3 and anti-CD28 antibodies in the absence and in the presence of DA and antagonists of DA-receptors at a concentration of 10-5 M.
Results: The level of DA was lower in MS patients during relapse than in patients during remission and in healthy subjects (p< 0.05). The percentages of Th17-cells and production of IL-17 and IFN-γ by PBMC were higher in patients in relapse compared to patients in remission or to the control group (p< 0.01). DA reduced IL-17 and IFN-γ production in all groups (p< 0.05). Blockade of D1-like receptors enhanced the inhibitory effect of DA on IL-17 production (p< 0.05) while blockade of D2-like receptors abolished the suppressive effect of DA in all groups. Blockade of D1-like receptors without the subsequent addition of DA reduced the production of IL-17 (p< 0.05) while blockade of D2-like receptors stimulated production of IL-17 in all groups (p< 0.05).
Conclusion: These data suggest an anti-inflammatory role for DA in MS which is mediated by D2-receptors.
Disclosure: There is nothing to disclose.
Abstract: P426
Type: Poster
Abstract Category: Pathology and pathogenesis of MS - Immunology
Introduction: Multiple sclerosis (MS) - chronic autoimmune disease of the CNS predominantly mediated by T-cells. Dopamine (DA) can participate in MS pathogenesis modulating immune cells activity and cytokine production.
Objective: To study the relationship between clinical impairment, DA concentration in the serum, quantitative characteristics of Тh17-cells, and to clarify the influence of DA on the function of Th17 cells.
Materials and methods: Data from 43 patients with relapsing-remitting MS and 20 healthy controls were included. Fourteen patients were examined during relapses, 29 during clinical remission. The DA concentration in the serum was measured by ELISA. Circulating Th17-cells were determined by flow cytometry (CD4+CD26+CD161+CD196+). The levels of interleukin-17 (IL-17) and interferon-gamma (IFN-γ) were studied by ELISA in supernatants of peripheral blood mononuclear cells (PBMC) stimulated with microbeads coated with anti-CD3 and anti-CD28 antibodies in the absence and in the presence of DA and antagonists of DA-receptors at a concentration of 10-5 M.
Results: The level of DA was lower in MS patients during relapse than in patients during remission and in healthy subjects (p< 0.05). The percentages of Th17-cells and production of IL-17 and IFN-γ by PBMC were higher in patients in relapse compared to patients in remission or to the control group (p< 0.01). DA reduced IL-17 and IFN-γ production in all groups (p< 0.05). Blockade of D1-like receptors enhanced the inhibitory effect of DA on IL-17 production (p< 0.05) while blockade of D2-like receptors abolished the suppressive effect of DA in all groups. Blockade of D1-like receptors without the subsequent addition of DA reduced the production of IL-17 (p< 0.05) while blockade of D2-like receptors stimulated production of IL-17 in all groups (p< 0.05).
Conclusion: These data suggest an anti-inflammatory role for DA in MS which is mediated by D2-receptors.
Disclosure: There is nothing to disclose.