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D2R agonist sumanirole in vitro inhibits CIA-induced bias of CD4⁺ T cells towards Th1 and Th17 phenotypes and D2R antagonist L-741,626 blocks this effect. A Protein expression of the specific transcription factors in CD4⁺ T cells. The left panel represents Western blotting bands and the right panel indicates quantitative data of the left panel. B Gene expression levels of the cytokines in CD4⁺ T cells. C-F Concentrations of the cytokines in supernatants of the activated CD4⁺ T cells. All the data were from five repeated experiments. **P < 0.01, versus control group; ##P < 0.01, versus CIA group; &&P < 0.01, versus CIA + sumanirole 10–6 M group
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Background
Dopamine is a neurotransmitter and has been found to regulate lymphocytes by acting on dopamine receptors (DRs). CD4⁺ T cells express all the five subtypes of DRs, D1R to D5R. Although CD4⁺ T cells have been involved in pathogenesis of rheumatoid arthritis (RA), roles of DRs expressed on these cells in RA are poorly understood. This stud...
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Introduction: Rheumatoid arthritis (RA) is a chronic inflammatory disorder with high prevalence among middle-aged women. Collagen-induced arthritis (CIA) is the most widely used animal model of RA, however, sex differences and long-term effects of CIA in mice are poorly described in the literature.
Aim: Therefore, the present study aimed to analyze...
Citations
... It is noteworthy that regulatory T cells, the main immunomodulatory cell population, express dopaminergic receptors ) and have shown neuroprotective effects in murine models of PD (Wang et al. 2023). While other populations of regulatory cells, including Bregs, CD8regs, IL-10-producing monocytes, and tolerogenic dendritic cells (DCs) have also been reported to express dopamine receptors , their role in controlling inflammation during PD has been poorly studied. ...
Whilst the contribution of peripheral and central inflammation to neurodegeneration in Parkinson’s disease and the role of the immune response in this disorder are well known, the effects of the anti-inflammatory response on the disease have not been described in depth. This study is aimed to assess the changes in the regulatory/inflammatory immune response in recently diagnosed, untreated PD patients and a year after. Twenty-one PD patients and 19 healthy controls were included and followed-up for 1 year. The levels of immunoregulatory cells (CD4+ Tregs, Bregs, and CD8+ Tregs); classical, nonclassical, and intermediate monocytes, and proinflammatory cells (Th1, Th2, and Th17) were measured by flow cytometry. Cytokine levels were determined by ELISA. Clinical follow-up was based on the Hoehn & Yahr and UDPRS scales. Our results indicate that the regulatory response in PD patients on follow-up was characterized by increased levels of active Tregs, functional Tregs, TR1, IL-10-producing functional Bregs, and IL-10-producing classical monocytes, along with decreased counts of Bregs and plasma cells. With respect to the proinflammatory immune response, peripheral levels of Th1 IFN-γ+ cells were decreased in treated PD patients, whilst the levels of CD4+ TBET+ cells, HLA-DR+ intermediate monocytes, IL-6, and IL-4 were increased after a 1-year follow-up. Our main finding was an increased regulatory T cell response after a 1-year follow-up and its link with clinical improvement in PD patients. In conclusion, after a 1-year follow-up, PD patients exhibited increased levels of regulatory populations, which correlated with clinical improvement. However, a persistent inflammatory environment and active immune response were observed.
