ArticleNature communications2017
TWEAK mediates inflammation in experimental atopic dermatitis and psoriasis.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.
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Who cites it
43 citing papers in PubMed, 1 synthesis or guideline pooled it, 78 citations in OpenAlex.
- Diagnostic value of TWEAK for predicting active lupus nephritis in patients with systemic lupus erythematosus: a systematic review and meta-analysis.Renal failure · 2021Pooled it
- Single-cell transcriptome reveals keratinocyte subclusters contributing to altered differentiation and inflammatory responses in atopic dermatitis.Nature communications · 2026Article
- Celastrol attenuates Th1- and Th2-driven skin inflammation in 2D and 3D in vitro models.Scientific reports · 2026Article
- Transcriptomic response toMicrobiology spectrum · 2026Article
- Role of LIGHT in the Inflammatory Mechanisms of Psoriasis via Upregulation of Proliferation and Cytokine Production of Keratinocytes.Immunity, inflammation and disease · 2026Article
- IL-27 signaling mediates skin inflammation in experimental psoriasis and atopic dermatitis.Cell & bioscience · 2026Article
- Longitudinal plasma proteomics identifies diagnostic and response-associated inflammatory and immune biomarkers in psoriasis following secukinumab therapy.Frontiers in immunology · 2026Article
- Differentiation defects reposition sebaceous glands as inflammatory instigators in the early pathogenesis of hidradenitis suppurativa.Frontiers in immunology · 2026Article
- Regulatory T Cells: Subtle and Promising Achilles' Heel of Psoriasis - Atherosclerosis Comorbidity.Mini reviews in medicinal chemistry · 2026Review
- Circulating inflammatory proteins as pathogenic mediators and potential therapeutic targets in myasthenia gravis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025Article
- Synergistic effects of LCN2 and TWEAK on the progression of psoriasis.Cellular & molecular immunology · 2025Article
- Comparison of CD30L and OX40L Reveals CD30L as a Promising Therapeutic Target in Atopic Dermatitis.Allergy · 2025Article
- Single-cell RNA sequencing reveals the impaired epidermal differentiation and pathological microenvironment in diabetic foot ulcer.Burns & trauma · 2025Article
- Targeting the TNF and TNFR superfamilies in autoimmune disease and cancer.Nature reviews. Drug discovery · 2024Review
- Review
- Pre-diagnostic plasma inflammatory proteins and risk of hepatocellular carcinoma in three population-based cohort studies from the United States and the United Kingdom.International journal of cancer · 2024Article
- Role of fibroblasts in nonfibrotic autoimmune skin diseases.Molecular medicine (Cambridge, Mass.) · 2024Review
- Anti-inflammatory Capacity of a Medicinal herb extract,Heliyon · 2024Article
- Single-cell landscape of bronchoalveolar immune cells in patients with immune checkpoint inhibitor-related pneumonitis.NPJ precision oncology · 2024Article
- The neuroscience of itch in relation to transdiagnostic psychological approaches.Scientific reports · 2024Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Atopic dermatitis (AD) and psoriasis are driven by alternate type 2 and type 17 immune responses, but some proteins might be critical to both diseases. Here we show that a deficiency of the TNF superfamily molecule TWEAK (TNFSF12) in mice results in defective maintenance of AD-specific T helper type 2 (Th2) and psoriasis-specific Th17 cells in the skin, and impaired expression of disease-characteristic chemokines and cytokines, such as CCL17 and TSLP in AD, and CCL20 and IL-19 in psoriasis. The TWEAK receptor, Fn14, is upregulated in keratinocytes and dermal fibroblasts, and TWEAK induces these cytokines and chemokines alone and in synergy with the signature T helper cytokines of either disease, IL-13 and IL-17. Furthermore, subcutaneous injection of recombinant TWEAK into naive mice induces cutaneous inflammation with histological and molecular signs of both diseases. TWEAK is therefore a critical contributor to skin inflammation and a possible therapeutic target in AD and psoriasis.
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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.