ArticleClinical reviews in allergy & immunology2017
Response to Treatment with TNFα Inhibitors in Rheumatoid Arthritis Is Associated with High Levels of GM-CSF and GM-CSF
Article in Clinical reviews in allergy & immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 35 citations in OpenAlex.
- Immunization with detoxified TNFα elicits neutralizing antibodies and ameliorates inflammatory shock and autoimmune arthritis in mice.Frontiers in immunology · 2026Article
- Predictive biomarkers for precision treatment in rheumatoid arthritis: are we there yet?Frontiers in pharmacology · 2026Review
- From immunosuppression to immune reprogramming: is triptolide a potential "immune reset" agent in autoimmune diseases?Immunologic research · 2025Review
- Suberosin attenuates rheumatoid arthritis by repolarizing macrophages and inhibiting synovitis via the JAK/STAT signaling pathway.Arthritis research & therapy · 2025Article
- GM-CSFTheranostics · 2025Review
- Plasma Cytokines for the Prediction of the Effectiveness of TNFα Inhibitors Etanercept, Infliximab, and Adalimumab in the Treatment of Psoriasis.Journal of clinical medicine · 2024Article
- Contribution of adaptive immunity to human COPD and experimental models of emphysema.Physiological reviews · 2023Review
- Past, Present and (Foreseeable) Future of Biological Anti-TNF Alpha Therapy.Journal of clinical medicine · 2023Review
- Chemokines and chemokine receptors as promising targets in rheumatoid arthritis.Frontiers in immunology · 2023Review
- Mechanisms underlying DMARD inefficacy in difficult-to-treat rheumatoid arthritis: a narrative review with systematic literature search.Rheumatology (Oxford, England) · 2022Review
- Plasma interleukin-23 and circulating IL-17AArthritis research & therapy · 2022Article
- Metabolic requirements of Th17 cells and of B cells: Regulation and defects in health and in inflammatory diseases.Frontiers in immunology · 2022Review
- Abdominal vagus nerve stimulation alleviates collagen-induced arthritis in rats.Frontiers in neuroscience · 2022Article
- Hypereosinophilic syndrome-a rare adverse event of anti-cytokine treatment in rheumatoid arthritis resolved after Janus kinase inhibitor therapy.Clinical rheumatology · 2020Review
- GM-CSF: A Promising Target in Inflammation and Autoimmunity.ImmunoTargets and therapy · 2020Review
- GM-CSF Primes Proinflammatory Monocyte Responses in Ankylosing Spondylitis.Frontiers in immunology · 2020Article
- Anti-TNF Therapy in Spondyloarthritis and Related Diseases, Impact on the Immune System and Prediction of Treatment Responses.Frontiers in immunology · 2019Review
- Autoimmunity in 2017.Clinical reviews in allergy & immunology · 2018Review
- TNF and granulocyte macrophage-colony stimulating factor interdependence mediates inflammation via CCL17.JCI insight · 2018Article
- Leveraging blood and tissue CD4+ T cell heterogeneity at the single cell level to identify mechanisms of disease in rheumatoid arthritis.Current opinion in immunology · 2017Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Biologic TNFα inhibitors are a mainstay treatment option for patients with rheumatoid arthritis (RA) refractory to other treatment options. However, many patients either do not respond or relapse after initially responding to these agents. This study was carried out to identify biomarkers that can distinguish responder from non-responder patients before the initiation of treatment. The level of cytokines in plasma and those produced by ex vivo T cells, B cells and monocytes in 97 RA patients treated with biologic TNFα inhibitors was measured before treatment and after 1 and 3 months of treatment by multiplex analyses. The frequency of T cell subsets and intracellular cytokines were determined by flow cytometry. The results reveal that pre-treatment, T cells from patients who went on to respond to treatment with biologic anti-TNFα agents produced significantly more GM-CSF than non-responder patients. Furthermore, immune cells from responder patients produced higher levels of IL-1β, TNFα and IL-6. Cytokine profiling in the blood of patients confirmed the association between high levels of GM-CSF and responsiveness to biologic anti-TNFα agents. Thus, high blood levels of GM-CSF pre-treatment had a positive predictive value of 87.5% (61.6 to 98.5% at 95% CI) in treated RA patients. The study also shows that cells from most anti-TNFα responder patients in the current cohort produced higher levels of GM-CSF and TNFα pre-treatment than non-responder patients. Findings from the current study and our previous observations that non-responsiveness to anti-TNFα is associated with high IL-17 levels suggest that the disease in responder and non-responder RA patients is likely to be driven/sustained by different inflammatory pathways. The use of biomarker signatures of distinct pro-inflammatory pathways could lead to evidence-based prescription of the most appropriate biological therapies for different RA patients.
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Registered trials
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