ArticleFrontiers in immunology2020
Cytokine Signature in Schnitzler Syndrome: Proinflammatory Cytokine Production Associated to Th Suppression.
Article in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 25 citations in OpenAlex.
- Paraprotein-Negative IL-1-Mediated Inflammatory Dermatosis: An Update on Schnitzler-Like Syndrome in the Absence of a Gammopathy.JID innovations : skin science from molecules to population health · 2025Article
- Neutrophilic Urticarial Dermatosis: A Window into Systemic Inflammation and Autoimmune Disorders.Clinical reviews in allergy & immunology · 2025Review
- Background and Clinical Features of a Unique and Mysterious Autoinflammatory Disease, Schnitzler Syndrome.International journal of molecular sciences · 2025Review
- Case report: Therapeutic use of bortezomib in a patient with Schnitzler syndrome.Frontiers in immunology · 2025Article
- Schnitzler Syndrome: Insights into Its Pathogenesis, Clinical Manifestations, and Current Management.Biomolecules · 2024Review
- Dermatologic Manifestations of Noninflammasome-Mediated Autoinflammatory Diseases.JID innovations : skin science from molecules to population health · 2023Review
- New insights on multigenic autoinflammatory diseases.Therapeutic advances in musculoskeletal disease · 2022Review
- Immunoglobulin M Monoclonal Gammopathies of Clinical Significance.Frontiers in oncology · 2022Review
- Clinical Presentation of Schnitzler's Syndrome: A Rare Autoimmune Disease.Journal of investigative medicine high impact case reportsArticle
Corrections and comments
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Authors and funding
25 authors at 19 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Schnitzler syndrome (SchS) is a rare autoinflammatory disease characterized by urticarial exanthema, bone and joint alterations, fever and monoclonal IgM gammopathy. Overactivation of the interleukin(IL)-1 system is reported, even though the exact pathophysiological pathways remain unknown. Objective: To determine Methods: We collected blood samples from thirty-six untreated or treated SchS. PBMCs were cultured with and without LPS or anti-CD3/CD28. Cytokine levels were evaluated in serum and cell culture supernatants using Luminex technology. Results: Spontaneous TNFα, IL-6, IL-1β, IL-1α, and IL-1RA release by PBMCs of SchS patients were higher than in controls. LPS-stimulation further induced the secretion of these cytokines. In contrast, after T-cell stimulation, TNFα, IL-10, IFNγ, IL-17A, and IL-4 production decreased in SchS patients compared to healthy controls, but less in treated patients. Whereas IL-1β serum level was not detected in most sera, IL-6, IL-10, and TNFα serum levels were higher in patients with SchS and IFNγ and IL-4 levels were lower. Of note, IL-6 decreased after treatment in SchS ( Conclusion: Our data strengthen the hypothesis of myeloid inflammation in SchS, mediated in particular by IL-1β, TNFα, and IL-6, associated with overproduction of the inhibitors IL-1RA and IL-10. In contrast, we observed a loss of Th1, Th2, and Th17 cell functionalities that tends to be reversed by anakinra.
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