ArticleClinical and experimental immunology2011
Tumour necrosis factor-like weak inducer of apoptosis (TWEAK), an important mediator of endothelial inflammation, is associated with the pathogenesis of Henoch-Schonlein purpura.
Article in Clinical and experimental immunology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
19 citing papers in PubMed, 44 citations in OpenAlex.
- The role ofFrontiers in immunology · 2025Article
- Co-Stimulation with TWEAK and TGF-β1 Induces Steroid-Insensitive TSLP and CCL5 Production in BEAS-2B Human Bronchial Epithelial Cells.International journal of molecular sciences · 2024Article
- MAP3K19 Affects TWEAK-Induced Response in Cultured Bronchial Epithelial Cells and Regulates Allergic Airway Inflammation in an Asthma Murine Model.Current issues in molecular biology · 2023Article
- Article
- Controversies in TWEAK-Fn14 signaling in skeletal muscle atrophy and regeneration.Cellular and molecular life sciences : CMLS · 2020Review
- Experimental atopic dermatitis is dependent on the TWEAK/Fn14 signaling pathway.Clinical and experimental immunology · 2020Article
- Serum levels of tumor necrosis factor-like weak inducer of apoptosis (TWEAK) in predicting the severity of acute pancreatitis.European journal of trauma and emergency surgery : official publication of the European Trauma Society · 2019Article
- Differential expression of long non-coding RNA and mRNA in children with Henoch-Schönlein purpura nephritis.Experimental and therapeutic medicine · 2019Article
- Fn14 deficiency ameliorates psoriasis-like skin disease in a murine model.Cell death & disease · 2018Article
- [Research advances in immunological pathogenesis of immunoglobulin A vasculitis].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2017Review
- TWEAK/Fn14 Activation Participates in Skin Inflammation.Mediators of inflammation · 2017Review
- Endothelial Response to Glucocorticoids in Inflammatory Diseases.Frontiers in immunology · 2016Review
- HPV Type 16 Infection Switches Keratinocytes from Apoptotic to Proliferative Fate under TWEAK/Fn14 Interaction.The Journal of investigative dermatology · 2015Article
- TWEAK enhances TGF-β-induced epithelial-mesenchymal transition in human bronchial epithelial cells.Respiratory research · 2015Article
- Increased serum levels of soluble vascular endothelial-cadherin in patients with systemic vasculitis.Rheumatology international · 2014Article
- TWEAK enhances E-selectin and ICAM-1 expression, and may contribute to the development of cutaneous vasculitis.PloS one · 2013Article
- Tumor necrosis factor-like weak inducer of apoptosis and its potential roles in lupus nephritis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2012Review
- Pediatric vasculitis.Current rheumatology reports · 2012Review
- TWEAK Progress in Dermatology: A Review.Indian journal of dermatologyReview
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumour necrosis factor-like weak inducer of apoptosis (TWEAK), a member of the tumour necrosis factor (TNF) family, has been implicated as a proinflammatory cytokine in many types of autoimmune and infectious diseases. However, information about TWEAK in dermatological diseases is limited. Herein, we investigated the role of TWEAK in patients with Henoch-Schonlein purpura (HSP) and the ability of TWEAK on chemokine production in the human dermal microvascular endothelial cell line (HMEC-1). Serum TWEAK levels in patients with HSP, together with patients with psoriasis vulgaris (PV) and atopic dermatitis (AD), were detected by enzyme-linked immunosorbent assay (ELISA). HMEC-1 cells were treated with TWEAK at concentrations ranging from 1 ng/ml to 100 ng/ml. Serum levels of TWEAK were elevated in patients with HSP in the acute stage but not in patients with PV or AD. Moreover, TWEAK levels were correlated with the severity of HSP. TWEAK markedly induced CCL5 and CXCL8 production at both mRNA and protein levels in HMEC-1 cells. In addition, TWEAK-stimulated HMEC-1 supernatant enhanced HL-60 or human acute monocytic leukaemia cell line (THP-1) cell migration. Finally, Western blot data revealed that TWEAK can induce rapid phosphorylation of inhibitor of κB-α (IκBα) in HMEC-1 cells. In conclusion, we show that serum levels of TWEAK were elevated in patients with acute stage HSP. TWEAK may act as a regulator of nuclear factor-κB (NF-κB) activation and chemokine production in human dermal microvascular endothelial cells, thus promoting leucocyte migration in cutaneous vasculitis.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.