ArticleJournal of inflammation research2026
Monocyte/Macrophage Subsets in the Peripheral Blood, Their Related Cytokines, and Circulating Markers of Fibrosis in Active Takayasu Arteritis and Longitudinal Changes Following Immunosuppressive Therapy.
Article in Journal of inflammation research, 2026. 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.
- Editorial: Insights into the diagnosis, pathogenesis and management of Takayasu arteritis.Frontiers in immunology · 2026Article
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: Takayasu arteritis (TAK) is a rare, stenosing large vessel vasculitis characterised by arterial wall fibrosis. Longitudinal changes in circulating monocyte/macrophage populations, which drive both inflammation and fibrosis in TAK, have not been studied. Patients and Methods: Circulating monocyte/macrophage populations, related cytokines, and markers of fibrosis were evaluated longitudinally in active TAK and compared with healthy controls. Flow cytometry was performed on peripheral blood mononuclear cells to identify overall CD14+CD66b-, M1-like, and M2-like monocytes/macrophages. Serum M1-like (TNF-α, IL-1β, IL-6, IP-10, IL-12p40, IL-23) and M2-like cytokines (IL-1RA, IL-10, CCL17) and circulating proteins indicating arterial wall fibrosis [plasma hyaluronic acid (HA), procollagen-III aminoterminal propeptide (PIIINP), tissue inhibitor of metalloproteinase 1 (TIMP-1), serum transforming growth factor-beta (TGF-β)] were estimated using cytokine bead array or ELISA. Mann-Whitney Results: Eighteen patients with active TAK and 8 age- and sex-similar healthy controls were recruited. Patients with active TAK had higher circulating overall, M1-like, and M2-like monocytes/macrophages than controls (p<0.001). M1-like cytokines TNF-⍺, IL-6, and IL-23, and M2-like cytokine IL-1RA were higher in active TAK than controls (p<0.001). Circulating markers of fibrosis HA and PIIINP were significantly elevated in active TAK than controls (p<0.05). Following immunosuppressive therapy, a significant decrease in overall and M1-like monocytes/macrophages and related cytokines (TNF-⍺, IL-1β, IL-6, IL-12p40, IP-10, IL-23) concomitant with an increase in M2-like monocytes/macrophages, related M2-like cytokines (IL-10, CCL17) and circulating markers of fibrosis (HA, TIMP-1, PIIINP, TGF-β) was observed (p<0.05). Conclusion: A transition from M1-like to M2-like monocyte/macrophage populations with an increase in circulating markers of fibrosis is seen in the peripheral blood following immunosuppressive therapy in active TAK. Future treatment strategies should evaluate a combination of anti-fibrotic agents with immunosuppressive therapy in TAK.
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