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Analysis of proinflammatory cytokine responses in Takayasu arteritis
Journal article   Peer reviewed

Analysis of proinflammatory cytokine responses in Takayasu arteritis

Filiz Ture Ozdemir, Fatma Alibaz-Oner, Ali Ugur Unal, Rabia Deniz, Gulsen Ozen, Imren Aydin-Tatli, Haner Direskeneli and Aysin Tulunay-Virlan
Archives of rheumatology, Vol.39(4), p.598
12/01/2024
DOI: 10.46497/ArchRheumatol.2024.10790
PMCID: PMC11883268
PMID: 40060124

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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[+ or -]15.5 years; range, 20 to 69 years) with TAK and 25 healthy controls (HCs; 11 females, 14 males; mean age: 39.1[+ or -]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-[gamma]), interleukin (IL)-17, IL-7, IL-21, and IL-22 levels. Results: Under Th17 cell-inducing conditions, IFN-[gamma] 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-[gamma] 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-[gamma] by [CD4.sup.+], [CD8.sup.+], and [gamma][[delta].sup.+] T cells and B cells was not found to be significantly different between TAK patients and HCs. No differences were observed between the subgroups of TAK according to disease activity or treatment in IL-17 and IFN-[gamma] production. Conclusion: This study supports cell-mediated cytotoxicity as the main pathogenetic mechanism of TAK. T cells express higher levels of IFN-[gamma] in TAK but not IL-17. Supernatant analysis indicated significantly higher IFN-[gamma] production, which significantly increased after induction, suggesting the contribution of different inflammatory cells (probably [CD8.sup.+] and [delta][[delta].sup.+] T cells) to IFN- [gamma] production in TAK. Keywords: Adaptive immunity, interferon-gamma, interleukin-17, Takayasu arteritis, T helper 17 cells.
 Biological Response Modifiers Interleukins Monoclonal Antibodies Analysis B cells Enzyme-linked immunosorbent assay Immune response Interferon Somatotropin T cells

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