ArticleThe Journal of investigative dermatology2015
TWEAK/Fn14 Signaling Involvement in the Pathogenesis of Cutaneous Disease in the MRL/lpr Model of Spontaneous Lupus.
Article in The Journal of investigative dermatology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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.
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Who cites it
32 citing papers in PubMed, 55 citations in OpenAlex.
- Single-cell transcriptome reveals keratinocyte subclusters contributing to altered differentiation and inflammatory responses in atopic dermatitis.Nature communications · 2026Article
- Mucosal-associated invariant T cells support IL-15-dependent Treg response in skin injury and promote resolution of skin inflammation.bioRxiv : the preprint server for biology · 2026Article
- Mechanisms of norcantharidin against renal tubulointerstitial fibrosis.Pharmacological reports : PR · 2024Review
- Lipocalin-2 drives neuropsychiatric and cutaneous disease in MRL/lpr mice.Frontiers in immunology · 2024Article
- Restoration of aberrant gene expression of monocytes in systemic lupus erythematosus via a combined transcriptome-reversal and network-based drug repurposing strategy.BMC genomics · 2023Article
- TWEAK functions with TNF and IL-17 on keratinocytes and is a potential target for psoriasis therapy.Science immunology · 2021Article
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- Tumor Necrosis Factor (TNF) Receptor Expression Determines Keratinocyte Fate upon Stimulation with TNF-Like Weak Inducer of Apoptosis.Mediators of inflammation · 2019Article
- Anti-double Stranded DNA Antibodies: Origin, Pathogenicity, and Targeted Therapies.Frontiers in immunology · 2019Review
- A protective Langerhans cell-keratinocyte axis that is dysfunctional in photosensitivity.Science translational medicine · 2018Article
- Fn14 deficiency ameliorates psoriasis-like skin disease in a murine model.Cell death & disease · 2018Article
- Mechanisms of neuropsychiatric lupus: The relative roles of the blood-cerebrospinal fluid barrier versus blood-brain barrier.Journal of autoimmunity · 2018Article
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- Topical TWEAK Accelerates Healing of Experimental Burn Wounds in Mice.Frontiers in pharmacology · 2018Article
- Human and Murine Evidence for Mechanisms Driving Autoimmune Photosensitivity.Frontiers in immunology · 2018Review
- The blood brain barrier and neuropsychiatric lupus: new perspectives in light of advances in understanding the neuroimmune interface.Autoimmunity reviews · 2017Review
- TWEAK mediates inflammation in experimental atopic dermatitis and psoriasis.Nature communications · 2017Article
- Beyond TNF: TNF superfamily cytokines as targets for the treatment of rheumatic diseases.Nature reviews. Rheumatology · 2017Review
- TWEAK/Fn14 Activation Participates in Ro52-Mediated Photosensitization in Cutaneous Lupus Erythematosus.Frontiers in immunology · 2017Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
Tumor necrosis factor (TNF)-like weak inducer of apoptosis (TWEAK, TNFSF12) and its sole receptor Fn14, belonging to the TNF ligand and receptor superfamilies respectively, are involved in cell survival and cytokine production. The role of TWEAK/Fn14 interactions in the pathogenesis of cutaneous lupus has not been explored. TWEAK treatment of murine PAM212 keratinocytes stimulated the secretion of RANTES via Fn14 and promoted apoptosis. Parthenolide, but not wortmanin or the MAPK inhibitor PD98059, significantly decreased production of RANTES, indicating that this effect of TWEAK is mediated via NF-κB signaling. UVB irradiation significantly upregulated the expression of Fn14 on keratinocytes in vitro and in vivo and increased RANTES production. MRL/lpr Fn14 knockout (KO) lupus mice were compared with MRL/lpr Fn14 wild-type (WT) mice to evaluate for any possible differences in the severity of cutaneous lesions and the presence of infiltrating immune cells. MRL/lpr Fn14 KO mice had markedly attenuated cutaneous disease as compared with their Fn14 WT littermates, as evidenced by the well-maintained architecture of the skin and significantly decreased skin infiltration of T cells and macrophages. Our data strongly implicate TWEAK/Fn14 signaling in the pathogenesis of the cutaneous manifestations in the MRL/lpr model of spontaneous lupus and suggest a possible target for therapeutic intervention.
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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.