ArticleArthritis research & therapy2022
Serum granulocyte-macrophage colony-stimulating factor (GM-CSF) is increased in patients with active radiographic axial spondyloarthritis and persists despite anti-TNF treatment.
Article in Arthritis research & therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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11 citing papers in PubMed, 11 citations in OpenAlex.
- CD200Nature communications · 2026Article
- Comparative Cytokine Profiles in Enthesitis-Related Arthritis and Adult Spondyloarthritis.Indian journal of pediatrics · 2026Article
- Tofacitinib repairs inflammation and mitochondrial dysregulation in GM-CSF-reprogrammed RA macrophages.Cellular & molecular immunology · 2026Article
- From IL-23/IL-17 to GM-CSF: how is the immuno-inflammatory continuum reshaped in spondyloarthritis?Frontiers in immunology · 2026Review
- Granulocyte-macrophage colony-stimulating factor may contribute to spondyloarthritis development in HLA-B27 transgenic rat by affecting conventional dendritic cells function.Arthritis research & therapy · 2025Article
- Bone metabolism and inflammatory biomarkers in radiographic and non-radiographic axial spondyloarthritis patients: a comprehensive evaluation.Frontiers in endocrinology · 2024Article
- Osteoimmunology of Spondyloarthritis.International journal of molecular sciences · 2023Review
- Interaction of S100A6 Protein with the Four-Helical Cytokines.Biomolecules · 2023Article
- JAK Inhibitors for the Treatment of Axial Spondyloarthritis.Mediterranean journal of rheumatology · 2023Review
- Uncovering the Underworld of Axial Spondyloarthritis.International journal of molecular sciences · 2023Review
- The Role of Neutrophils in Spondyloarthritis: A Journey across the Spectrum of Disease Manifestations.International journal of molecular sciences · 2023Review
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5 authors at 4 institutions in 2 countries.
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Abstract
backgroundAccumulating evidence supports the role of monocytes and neutrophils in radiographic axSpA (r-axSpA). Granulocyte-macrophage colony-stimulating factor (GM-CSF) is a growth factor for both leukocyte lineages and a pro-inflammatory cytokine activating myeloid cells and promoting osteoclastogenesis. It acts through the JAK-STAT pathway. We measured serum GM-CSF and markers of bone metabolism in patients with r-axSpA before and after anti-TNF treatment.
methodsPatients with active r-axSpA despite treatment with NSAIDs, all eligible for treatment with a biologic agent, were recruited. Healthy donors were sampled as controls. Serum was collected before (baseline) and after 4-6 months (follow-up) of anti-TNF treatment and the following molecules were measured with ELISA: GM-CSF, sclerostin (SOST), and dickkopf-1 (Dkk-1).
resultsTwelve r-axSpA patients (7 males, 5 females, median age 37 years) with a median disease duration of 1 year and 16 age- and sex-matched controls were included. At baseline, patients had mean BASDAI 6.3±2 and ASDAS 3.2±0.7, which decreased to 4.1±1.7 and 2.2±0.6 at follow-up, respectively. At baseline, r-axSpA patients had significantly higher mean serum levels of GM-CSF (150 vs 62pg/ml, p=0.049), significantly lower Dkk-1 (1228 vs 3052pg/ml, p=0.001), but similar levels of SOST (369 vs 544pg/ml, p=0.144) compared to controls. Anti-TNF treatment did not affect GM-CSF, Dkk-1, or SOST levels. Spearman correlation analysis showed that GM-CSF correlated positively with ASDAS at baseline (r=0.61, p=0.039), while no correlations were identified between bone markers (Dkk-1, SOST) on one hand and GM-CSF or disease activity indices on the other.
conclusionsGM-CSF is increased in patients with active AS and strongly correlates with disease activity. TNF inhibition does not affect GM-SCF levels, despite improving disease activity. GM-CSF may represent an important pathway responsible for residual inflammation during TNF blockade, but also a potential target of JAK inhibitors, explaining their efficacy in r-axSpA.
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