ArticleClinical and experimental immunology2014
Expression of cytokines, chemokines and other effector molecules in two prototypic autoinflammatory skin diseases, pyoderma gangrenosum and Sweet's syndrome.
Article in Clinical and experimental immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 88 papers, 2 of them syntheses that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
88 citing papers in PubMed, 2 syntheses or guidelines pooled it, 235 citations in OpenAlex.
- Molecular Characteristics of Sweet Syndrome: A Systematic Review.Experimental dermatology · 2024Pooled it
- Inflammatory arthritis-associated pyoderma gangrenosum: a systematic review.Clinical rheumatology · 2021Pooled it
- Cutaneous Manifestations of Primary Sjögren's Syndrome: Pyoderma Gangrenosum as a Rare Initial Presentation - A Case Report and Literature Review.Annals of African medicine · 2026Review
- Type I and II Interferon Signalling Characterizes the Transcriptional Landscape of Sweet Syndrome.Experimental dermatology · 2026Article
- Integrative Multi-Omics Analysis and Computational Modeling Identifying Shared Inflammatory Pathways and JAK Inhibitor Targets in PG and IBD.International journal of molecular sciences · 2026Article
- Subcutaneous Sweet Syndrome as an uncommon mucocutaneous manifestation in systemic lupus erythematosus: a case report and literature review.Immunologic research · 2026Review
- Successful Treatment of Refractory Sweet's Syndrome With Adalimumab in a Myelodysplastic Syndrome Patient.EJHaem · 2026Article
- Concurrent paraneoplastic dermatomyositis and Sweet syndrome.JAAD case reports · 2026Article
- Successful treatment of severe retroauricular pyoderma gangrenosum with upadacitinib in a patient with Crohn's disease and a history of cerebral venous sinus thrombosis.Therapeutic advances in gastroenterology · 2026Article
- Pyoderma gangrenosum: pathogenetic mechanisms and their implications for treatment.Seminars in immunopathology · 2025Review
- Keratinocyte-neutrophil interactions revealed as targetable drivers of sustained inflammation in Sweet syndrome.The Journal of clinical investigation · 2025Article
- Sweet Syndrome-like Dermatosis as a Precursor to Overlapping Hematologic Malignancies: A Case Report and Review.Journal of clinical medicine · 2025Review
- Disrupted Redox Regulation and Inflammatory Response in Pyoderma Gangrenosum.Life (Basel, Switzerland) · 2025Article
- The Role of IL-17 in Systemic Autoinflammatory Diseases: Mechanisms and Therapeutic Perspectives.Clinical reviews in allergy & immunology · 2025Review
- Resolution of Pyoderma Gangrenosum During Adjuvant Breast Cancer Therapy.Journal of clinical medicine · 2025Article
- Paraneoplastic Dermatoses: A Clue for Underlying Malignancies.Journal of clinical medicine · 2025Review
- Anti-IL 17 biologics and pyoderma gangrenosum - therapeutic or causal?Archives of dermatological research · 2025Review
- Increased Inflammatory Responses in Patients With Active Disseminated Non-Tuberculous Mycobacterial Infection and High Anti-Interferon-Gamma Autoantibodies.Immune network · 2024Article
- Monoclonal Antibodies in the Management of Inflammation in Wound Healing: An Updated Literature Review.Journal of clinical medicine · 2024Review
- The Pathophysiology and Treatment of Pyoderma Gangrenosum-Current Options and New Perspectives.International journal of molecular sciences · 2024Review
28 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issuedCorrigendum.2015
Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pyoderma gangrenosum (PG) and Sweet's syndrome (SS) are two inflammatory skin diseases presenting with painful ulcers and erythematous plaques, respectively; both disorders have a debilitating clinical behaviour and PG is potentially life-threatening. Recently, PG and SS have been included among the autoinflammatory diseases, which are characterized by recurrent episodes of sterile inflammation, without circulating autoantibodies and autoreactive T cells. However, an autoinflammatory pattern clearly supporting this inclusion has never been demonstrated. We studied 16 patients with PG, six with SS and six controls, evaluating, using a sandwich-based protein antibody array method, the expression profile of inflammatory effector molecules in PG, SS and normal skin. The expressions of interleukin (IL)-1 beta and its receptor I were significantly higher in PG (P = 0·0001 for both) and SS (P = 0·004-0·040) than in controls. In PG, chemokines such as IL-8 (P = 0·0001), chemokine (C-X-C motif) ligand (CXCL) 1/2/3 (P = 0·002), CXCL 16 (P = 0·003) and regulated upon activation normal T cell expressed and secreted (RANTES) (P = 0·005) were over-expressed. In SS, IL-8 (P = 0·018), CXCL 1/2/3 (P = 0·006) and CXCL 16 (P = 0·036) but not RANTES were over-expressed, suggesting that chemokine-mediated signals are lower than in PG. Fas/Fas ligand and CD40/CD40 ligand systems were over-expressed in PG (P = 0·0001 for Fas, P = 0·009 for Fas ligand, P = 0·012 for CD40, P = 0·0001 for CD40 ligand), contributing to tissue damage and inflammation, while their role seems to be less significant in SS. Over-expression of cytokines/chemokines and molecules amplifying the inflammatory network supports the view that PG and SS are autoinflammatory diseases. The differences in expression profile of inflammatory effectors between these two disorders may explain the stronger local aggressiveness in PG than SS.
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Registered trials
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