ArticleThe American journal of pathology2009
Fn14-TRAIL, a chimeric intercellular signal exchanger, attenuates experimental autoimmune encephalomyelitis.
Article in The American journal of pathology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 29 citations in OpenAlex.
- TWEAK-Fn14: a promising target for cardio-cerebrovascular diseases and brain-heart syndrome.Frontiers in immunology · 2025Review
- Mendelian randomization and colocalization analysis reveal novel drug targets for myasthenia gravis.Human genomics · 2024Article
- Apoptotic cell death in disease-Current understanding of the NCCD 2023.Cell death and differentiation · 2023Review
- Regulation of Neuroinflammation: What Role for the Tumor Necrosis Factor-Like Weak Inducer of Apoptosis/Fn14 Pathway?Frontiers in immunology · 2017Review
- Onto better TRAILs for cancer treatment.Cell death and differentiation · 2016Review
- TNF-like weak inducer of apoptosis promotes blood brain barrier disruption and increases neuronal cell death in MRL/lpr mice.Journal of autoimmunity · 2015Article
- Role of Tumor Necrosis Factor Superfamily in Neuroinflammation and Autoimmunity.Frontiers in immunology · 2015Review
- Highly efficient, in-vivo Fas-mediated apoptosis of B-cell lymphoma by hexameric CTLA4-FasL.Journal of hematology & oncology · 2014Article
- A further TWEAK to multiple sclerosis pathophysiology.Molecular neurobiology · 2014Review
- TWEAK/Fn14 Axis-Targeted Therapeutics: Moving Basic Science Discoveries to the Clinic.Frontiers in immunology · 2013Article
- The TWEAK-Fn14 system as a potential drug target.British journal of pharmacology · 2013Review
- Amelioration of autoimmune neuroinflammation by the fusion molecule Fn14·TRAIL.Journal of neuroinflammation · 2013Article
- Article
- A single intrathecal injection of DNA and an asymmetric cationic lipid as lipoplexes ameliorates experimental autoimmune encephalomyelitis.Molecular pharmaceutics · 2011Article
- The death-promoting molecule tumour necrosis factor-related apoptosis inducing ligand (TRAIL) is not required for the development of peripheral lymphopenia or granuloma necrosis during infection with virulent Mycobacterium avium.Clinical and experimental immunology · 2011Article
- Neutralization of tumor necrosis factor-related apoptosis-inducing ligand reduces spinal cord injury damage in mice.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2010Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Hallmarks of the pathogenesis of autoimmune encephalomyelitis include perivascular infiltration of inflammatory cells into the central nervous system, multifocal demyelination in the brain and spinal cord, and focal neuronal degeneration. Optimal treatment of this complex disease will ultimately call for agents that target the spectrum of underlying pathogenic processes. In the present study, Fn14-TRAIL is introduced as a unique immunotherapeutic fusion protein that is designed to exchange and redirect intercellular signals within inflammatory cell networks, and, in so doing, to impact multiple pathogenic events and yield a net anti-inflammatory effect. In this soluble protein product, a Fn14 receptor component (capable of blocking the pro-inflammatory TWEAK ligand) is fused to a TRAIL ligand (capable of inhibiting activated, pathogenic T cells). Sustained Fn14-TRAIL expression was obtained in vivo using a transposon-based eukaryotic expression vector. Fn14-TRAIL expression effectively prevented chronic, nonremitting, paralytic disease in myelin oligodendrocyte glycoprotein-challenged C57BL/6 mice. Disease suppression in this model was reflected by decreases in the clinical score, disease incidence, nervous tissue inflammation, and Th1, Th2, and Th17 cytokine responses. Significantly, the therapeutic efficacy of Fn14-TRAIL could not be recapitulated simply by administering its component parts (Fn14 and TRAIL) as soluble agents, either alone or in combination. Its functional pleiotropism was manifest in its additional ability to attenuate the enhanced permeability of the blood-brain barrier that typically accompanies autoimmune encephalomyelitis.
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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.