2022
DOI: 10.1080/25785826.2022.2094593
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Istradefylline, an adenosine A2a receptor antagonist, inhibits the CD4 + T-cell hypersecretion of IL-17A and IL-8 in humans

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Cited by 5 publications
(4 citation statements)
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“…In this study, we confirmed that an A2aR agonist (PSB0777) induced IL-17A hypersecretion by TCR-activated CD4 + T cells not only in humans ( Tokano et al, 2022 ) but also in mice; this hypersecretion was suppressed by an A2aR antagonist (Istradefylline). In addition, and to the best of our knowledge, we reveal for the first time that inhibitors of the Gs downstream signaling pathway AC-cAMP-PKA-CREB also inhibit adenosine-mediated IL-17A hypersecretion by TCR-activated Th17 cells in mice ( Fig.…”
Section: Discussionsupporting
confidence: 75%
See 1 more Smart Citation
“…In this study, we confirmed that an A2aR agonist (PSB0777) induced IL-17A hypersecretion by TCR-activated CD4 + T cells not only in humans ( Tokano et al, 2022 ) but also in mice; this hypersecretion was suppressed by an A2aR antagonist (Istradefylline). In addition, and to the best of our knowledge, we reveal for the first time that inhibitors of the Gs downstream signaling pathway AC-cAMP-PKA-CREB also inhibit adenosine-mediated IL-17A hypersecretion by TCR-activated Th17 cells in mice ( Fig.…”
Section: Discussionsupporting
confidence: 75%
“…In addition, A2bR and A3R also signals the Gq protein, which in turn activates phospholipase C. In an immunological context, adenosine receptors are expressed by various immune cells, including T cells and APCs ( Junger, 2011 ). With respect to the effect of adenosine on Th cells, previous studies show that adenosine induces hypersecretion of IL-17A by human CD4 + T cells treated with an A2aR agonist (PSB0777) ( Tokano et al, 2022 ), as well as inducing Th17 differentiation via activation of A2bR on murine CD4 + T cells ( Wilson et al, 2011 ). However, the signaling pathway (downstream of adenosine-mediated IL-17A hypersecretion by CD4 + T cells and immune subsets) that induces adenosine-mediated IL-17A hypersecretion is unclear.…”
Section: Introductionmentioning
confidence: 99%
“…Furthermore, infiltrated CD39 + Th17 cells in the TME are proportional to poor clinical outcomes in cancer patients [60,61]. Interestingly, adenosine and an A 2A R agonist (PSB0777) promoted IL-17A and IL-8 production from human peripheral blood mononuclear cells in response to Candida albicans stimulation, suggesting a role for the adenosine/A 2A R pathway in Th17 cell differentiation [62]. In addition, in vivo experiments in mice showed that A 2B R promotes Th17 differentiation by augmenting IL-6 production by DCs, independent of intracellular cAMP, suggesting a different mechanism for Th17 cell differentiation by A 2B R [63].…”
Section: Effector Cd4 + T Helper Cellsmentioning
confidence: 99%
“…The research has focused on vaccines, antibody therapy, and immune-mediated therapies to clear abnormal protein aggregates. There are several ongoing clinical trials and, in 2019, FDA approved the drug istradefylline (Nourianz) (Administration USFaD 2019 ), a selective adenosine A2a receptor antagonist that inhibits T CD4 cell hypersecretion of IL-17A and IL-8 (Tokano et al 2022 ). Considering other therapies targeting inflammation, as previously mentioned, non-steroidal anti-inflammatory drugs were correlated with reduced risk of developing PD (Wahner et al 2007 ), while there are no grand-scale clinical trials to confirm this association.…”
Section: Inflammation As a Target For Parkinson’s Diseasementioning
confidence: 99%