Soluble programmed cell death-1 is increased in axial spondyloarthritis and present at the local site of pathology.
[OBJECTIVE] The combination of bone destruction and new bone formation is characteristic of spondyloarthritis.
APA
Ahrenfeldt E, Hvid M, et al. (2026). Soluble programmed cell death-1 is increased in axial spondyloarthritis and present at the local site of pathology.. Scandinavian journal of rheumatology, 1-6. https://doi.org/10.1080/03009742.2025.2599026
MLA
Ahrenfeldt E, et al.. "Soluble programmed cell death-1 is increased in axial spondyloarthritis and present at the local site of pathology.." Scandinavian journal of rheumatology, 2026, pp. 1-6.
PMID
41572845
Abstract
[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.