ArticleArchives of rheumatology2024
Analysis of proinflammatory cytokine responses in Takayasu arteritis.
Article in Archives of rheumatology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objectives: This study aimed to investigate the expression of proinflammatory cytokines under long-term T helper (Th) 17 cell inducing conditions in Takayasu arteritis (TAK), a granulomatous vasculitis with adaptive immune responses. Patients and methods: This cross-sectional study was conducted between May 2014 and April 2017. Peripheral blood mononuclear cells from 25 patients (23 females, 2 males; mean age: 42.7±15.5 years; range, 20 to 69 years) with TAK and 25 healthy controls (HCs; 11 females, 14 males; mean age: 39.1±9.3 years; range, 21 to 64 years) were cultured in Th17 cell-inducing conditions for six days. Cultured cells were stained with conjugated monoclonal antibodies to determine the intracellular cytokine secretion by flow cytometry. Supernatant samples were measured with sandwich enzyme-linked immunosorbent assay for interferon-gamma (IFN-γ), interleukin (IL)-17, IL-7, IL-21, and IL-22 levels. Results: Under Th17 cell-inducing conditions, IFN-γ secretion was significantly higher in the TAK group compared to HCs (p<0.005). Unstimulated serum cytokine levels showed no differences between the TAK and HC groups, except for IL-7. Both IL-17 and IFN-γ secretion showed significant increases in TAK and IL-17 secretion in HCs in comparison of unstimulated and stimulated samples for each individual (p values, 0.022, 0.005, and 0.016, respectively). The production of IL-17 and IFN-γ by CD4 Conclusion: This study supports cell-mediated cytotoxicity as the main pathogenetic mechanism of TAK. T cells express higher levels of IFN-γ in TAK but not IL-17. Supernatant analysis indicated significantly higher IFN-γ production, which significantly increased after induction, suggesting the contribution of different inflammatory cells (probably CD8
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