ArticleAllergy2024
TNF-like weak inducer of apoptosis inhibition is comparable to IL-13 blockade in ameliorating atopic dermatitis inflammation.
Article in Allergy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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.
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
6 citing papers in PubMed, 10 citations in OpenAlex.
- Article
- A genome-wide pleiotropy study between atopic dermatitis and neuropsychiatric disorders.Human genomics · 2025Article
- Comparison of CD30L and OX40L Reveals CD30L as a Promising Therapeutic Target in Atopic Dermatitis.Allergy · 2025Article
- Integrative Keratinocyte Responses to TWEAK with IL-13 and IL-22 Reveal Pathogenic Transcriptomes Associated with Atopic Dermatitis.The Journal of investigative dermatology · 2024Article
- Sodium Propionate Alleviates Atopic Dermatitis by Inhibiting Ferroptosis via Activation of LTBP2/FABP4 Signaling Pathway.Journal of inflammation research · 2024Article
- Elucidating the role of tumor-associated ALOX5+ mast cells with transformative function in cervical cancer progression via single-cell RNA sequencing.Frontiers in immunology · 2024Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
backgroundTargeting IL-13 is highly efficacious in patients with Th2-biased atopic dermatitis (AD), but inhibition of other inflammatory molecules might also limit disease. We investigated the importance of the TNF family cytokine TNF-like weak inducer of apoptosis (TWEAK; TNFSF12) to keratinocyte dysregulation and the pathogenesis of AD in mice and also tested if blocking TWEAK has a similar therapeutic effect as targeting IL-13.
methodsConditional knockout mice lacking Fn14 (TNFRSF12A), the receptor for TWEAK, only in keratinocytes, were repetitively sensitized with house dust mite allergen and analyzed for AD-like skin inflammation. To determine the translational potential, wild-type mice with AD were therapeutically treated with anti-TWEAK and/or anti-IL-13 antibodies, and skin inflammation was assessed.
resultsMice deficient in Fn14 in keratinocytes were resistant to developing maximal clinical features of AD, exhibiting reduced epidermal hyperplasia and dermal thickening, less skin infiltration of immune cells, and downregulated inflammatory gene expression. Moreover, therapeutic neutralization of TWEAK in wild-type mice with AD reduced all of the pathological features to a comparable extent as blocking IL-13.
conclusionsThe activity of TWEAK in keratinocytes contributes to AD development, and neutralizing TWEAK represents a future potential therapeutic option in human AD similar to targeting IL-13.
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Registered trials
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.