Scandinavian journal of rheumatology · 2026
Soluble programmed cell death-1 is increased in axial spondyloarthritis and present at the local site of pathology.
СтатьяНазвание и аннотация: Перевод в очереди
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Ahrenfeldt E, Hvid M, Jurik A G, Syrbe U, Poddubnyy D, Østgård R, Deleuran B, Greisen S R
Аннотация
OBJECTIVE: The combination of bone destruction and new bone formation is characteristic of spondyloarthritis. The proinflammatory cytokine interleukin-17A (IL-17A) is known to be central to the disease pathology, but immune regulatory mechanisms are poorly understood. We investigate the programmed cell death-1 (PD-1) pathway in patients with axial spondyloarthritis (axSpA) and the relationship between PD-1 and IL-17A.
METHOD: We analysed blood and synovial fluid from patients with long-standing axSpA and newly diagnosed patients undergoing 1 year of adalimumab treatment. We measured soluble programmed cell death-1 (sPD-1) and sPD ligand-2 (sPD-L2) levels and investigated their correlation with disease activity markers. Surface expression of PD-1 on lymphocytes was determined, and production of IL-17A in the presence of recombinant human (rh) PD-1 was investigated. Facet joint biopsies from axSpA patients undergoing surgery were stained for the presence of PD-1 and C-C chemokine receptor-6 (CCR6).
RESULTS: Plasma levels of sPD-1 and sPD-L2 were increased in both early and long-standing axSpA, but unaffected by 1 year of adalimumab treatment, and levels did not correlate with disease activity scores or progression. PD-1 expression was increased on synovial fluid mononuclear cells. Compared with peripheral blood mononuclear cells from healthy controls, those from axSpA patients produced more IL-17A when cultured with rhPD-1. PD-1 and CCR6 were present in facet joint biopsies.
CONCLUSION: We suggest a dual role for the PD-1 pathway in the pathogenesis of axSpA, acting in the inflamed microenvironment, with sPD-1 being suggestive of continued low immune activation.
METHOD: We analysed blood and synovial fluid from patients with long-standing axSpA and newly diagnosed patients undergoing 1 year of adalimumab treatment. We measured soluble programmed cell death-1 (sPD-1) and sPD ligand-2 (sPD-L2) levels and investigated their correlation with disease activity markers. Surface expression of PD-1 on lymphocytes was determined, and production of IL-17A in the presence of recombinant human (rh) PD-1 was investigated. Facet joint biopsies from axSpA patients undergoing surgery were stained for the presence of PD-1 and C-C chemokine receptor-6 (CCR6).
RESULTS: Plasma levels of sPD-1 and sPD-L2 were increased in both early and long-standing axSpA, but unaffected by 1 year of adalimumab treatment, and levels did not correlate with disease activity scores or progression. PD-1 expression was increased on synovial fluid mononuclear cells. Compared with peripheral blood mononuclear cells from healthy controls, those from axSpA patients produced more IL-17A when cultured with rhPD-1. PD-1 and CCR6 were present in facet joint biopsies.
CONCLUSION: We suggest a dual role for the PD-1 pathway in the pathogenesis of axSpA, acting in the inflamed microenvironment, with sPD-1 being suggestive of continued low immune activation.