ArticleThe American Journal of dermatopathology2011
An epidermotypic model of interface dermatitis reveals individual functions of fas ligand and gamma interferon in hypergranulosis, cytoid body formation, and gene expression.
Article in The American Journal of dermatopathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
4 citing papers in PubMed, 8 citations in OpenAlex.
- Clinical and immunopathological spectrum of immunoglobulin M pemphigoid: a multicenter case series.Journal der Deutschen Dermatologischen Gesellschaft = Journal of the German Society of Dermatology : JDDG · 2025Article
- Immunostimulatory Endogenous Nucleic Acids Perpetuate Interface Dermatitis-Translation of Pathogenic Fundamentals Into anFrontiers in immunology · 2020Review
- Immune response patterns in non-communicable inflammatory skin diseases.Journal of the European Academy of Dermatology and Venereology : JEADV · 2018Review
- Fas/Fas ligand mediates keratinocyte death in sunitinib-induced hand-foot skin reaction.The Journal of investigative dermatology · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Analysis of complex cutaneous reactions using animal models allows for the identification of essential or modulatory participants, that is, cyto- and chemokines or adhesion molecules. However, complex whole animal modeling is bound to obscure some specific contributions of individual players. Mouse models suggest that expression of Fas ligand (FasL) by donor T cells is essential for the cutaneous acute graft-versus-host reaction (aGvHR), a major complication after allogeneic hematopoietic stem cell transplantation. The role of FasL/Fas in human cutaneous GvHR is not known. To understand the mechanisms of cytotoxicity and inflammation in human cutaneous GvHR, we developed an organotypic model using reconstructed human epidermis (RHE) that was exposed to FasL, gamma-interferon (IFNγ), or both. The model recapitulated key histological hallmarks of cutaneous aGvHR, including interface dermatitis, appearance of cytoid bodies, hypergranulosis, and expression of ICAM-1. Cytoid body formation and expression of ICAM-1 were attributable entirely to IFNγ, whereas hypergranulosis was triggered by FasL. Both FasL and IFNγ triggered vacuolar degeneration of keratinocytes. The validity of the RHE model of GvHR was demonstrated by histological correlation with biopsied skin from patients with acute graft-versus-host disease. FasL and IFNγ each elicited potent and specific proinflammatory genomic responses in RHE. Inhibition of caspase activity dramatically augmented the FasL-induced proinflammatory responses, suggesting an "apoptosis-versus-inflammation" antagonism in cutaneous aGvHR and other lichenoid dermatoses.
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What OpenQuestion holds
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.