Clinical and experimental rheumatology · 2026
Dynamics of interleukin-23/interleukin-17 axis and type 1 regulatory T cells across disease stages in axial spondyloarthritis.
СтатьяНазвание и аннотация: Перевод в очереди
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Yeo Jina, Kim Min-Gang, Heo Su Young, Yang Yeonsoo, Seo Mi Ryoung, Choi Hyo-Jin, Jung Yunjae, Lee Eun Young, Baek Han Joo
Аннотация
OBJECTIVES: The interleukin (IL)-23/IL-17 pathway is central to the pathogenesis of axial spondyloarthritis (axSpA); however, treatments targeting IL-23 have shown inconsistent effectiveness across spondyloarthritis subtypes. We hypothesised that the IL-23/IL-17 axis varies with disease stage and is modulated by its regulatory counterparts, such as type 1 regulatory T (Tr1) cells.
METHODS: Serum levels of IL-17A and IL-23, along with peripheral CD4+IL-17A+ cells, monocytes (CD14+HLA-DR+), dendritic cells (DCs, CD11c+HLA-DR+), and Tr1 cells (CD4+CD49b+LAG3+FoxP3-IL-10+), were analysed in 20 patients with non-radiographic axSpA (nr-axSpA) and 24 with radiographic axSpA (r-axSpA) using enzyme-linked immunosorbent assay and flow cytometry. Additionally, we assessed IL-17A production by healthy CD4+ T cells stimulated by monocyte-derived DCs (moDCs) from patients with axSpA through co-culture experiments.
RESULTS: Patients with nr-axSpA had higher serum IL-23 levels (p=0.014), whereas IL-17A levels were comparable between both groups (p=0.912). Peripheral DCs from the nr-axSpA group produced more IL-23 (p=0.010), while no significant differences were observed in Th17 cell proportions (p>0.05). MoDCs from patients with nr-axSpA induced higher pro-inflammatory cytokine production in healthy CD4+ T cells than those from patients with r-axSpA (p<0.05). Notably, Tr1 cells were reduced in the nr-axSpA group (p=0.025), and IL-10 selectively suppressed IL-23 production by nr-axSpA moDCs (p=0.236).
CONCLUSIONS: These findings indicate that IL-23-associated immune activity may be relatively more prominent in early axSpA and that differences in Tr1 cell-related regulation across disease stages could contribute to this pattern.
METHODS: Serum levels of IL-17A and IL-23, along with peripheral CD4+IL-17A+ cells, monocytes (CD14+HLA-DR+), dendritic cells (DCs, CD11c+HLA-DR+), and Tr1 cells (CD4+CD49b+LAG3+FoxP3-IL-10+), were analysed in 20 patients with non-radiographic axSpA (nr-axSpA) and 24 with radiographic axSpA (r-axSpA) using enzyme-linked immunosorbent assay and flow cytometry. Additionally, we assessed IL-17A production by healthy CD4+ T cells stimulated by monocyte-derived DCs (moDCs) from patients with axSpA through co-culture experiments.
RESULTS: Patients with nr-axSpA had higher serum IL-23 levels (p=0.014), whereas IL-17A levels were comparable between both groups (p=0.912). Peripheral DCs from the nr-axSpA group produced more IL-23 (p=0.010), while no significant differences were observed in Th17 cell proportions (p>0.05). MoDCs from patients with nr-axSpA induced higher pro-inflammatory cytokine production in healthy CD4+ T cells than those from patients with r-axSpA (p<0.05). Notably, Tr1 cells were reduced in the nr-axSpA group (p=0.025), and IL-10 selectively suppressed IL-23 production by nr-axSpA moDCs (p=0.236).
CONCLUSIONS: These findings indicate that IL-23-associated immune activity may be relatively more prominent in early axSpA and that differences in Tr1 cell-related regulation across disease stages could contribute to this pattern.