ArticleProceedings of the National Academy of Sciences of the United States of America1996
A polygenic mouse model of psoriasiform skin disease in CD18-deficient mice.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed, 86 citations in OpenAlex.
- The Role of LFA-1 for the Differentiation and Function of Regulatory T Cells-Lessons Learned from Different Transgenic Mouse Models.International journal of molecular sciences · 2023Review
- Impaired Treg-DC interactions contribute to autoimmunity in leukocyte adhesion deficiency type 1.JCI insight · 2022Article
- Mouse Models of Psoriasis: A Comprehensive Review.The Journal of investigative dermatology · 2022Review
- New Frontiers in Psoriatic Disease Research, Part I: Genetics, Environmental Triggers, Immunology, Pathophysiology, and Precision Medicine.The Journal of investigative dermatology · 2021Review
- T-Cell Adhesion in Healthy and Inflamed Skin.JID innovations : skin science from molecules to population health · 2021Review
- Molecular Insights Into Neutrophil Biology From the Zebrafish Perspective: Lessons From CD18 Deficiency.Frontiers in immunology · 2021Article
- Research Techniques Made Simple: Murine Models of Human Psoriasis.The Journal of investigative dermatology · 2018Review
- Models in the Research Process of Psoriasis.International journal of molecular sciences · 2017Review
- Psoriasiform skin disease in transgenic pigs with high-copy ectopic expression of human integrins α2 and β1.Disease models & mechanisms · 2017Article
- Cross Talk between Proliferative, Angiogenic, and Cellular Mechanisms Orchestred by HIF-1α in Psoriasis.Mediators of inflammation · 2015Review
- The integrin adhesome: from genes and proteins to human disease.Nature reviews. Molecular cell biology · 2014Review
- Susceptibility to lethal cerebral malaria is regulated by epistatic interaction between chromosome 4 (Berr6) and chromosome 1 (Berr7) loci in mice.Genes and immunity · 2013Article
- Animal models of skin disease for drug discovery.Expert opinion on drug discovery · 2013Review
- Psoriasis: what we have learned from mouse models.Nature reviews. Rheumatology · 2010Review
- TGF-beta-dependent suppressive function of Tregs requires wild-type levels of CD18 in a mouse model of psoriasis.The Journal of clinical investigation · 2008Article
- Article
- Macrophages and neutrophils are the targets for immune suppression by glucocorticoids in contact allergy.The Journal of clinical investigation · 2007Article
- Misbehaving macrophages in the pathogenesis of psoriasis.The Journal of clinical investigation · 2006Article
- Activated macrophages are essential in a murine model for T cell-mediated chronic psoriasiform skin inflammation.The Journal of clinical investigation · 2006Article
- Pathogenic role for skin macrophages in a mouse model of keratinocyte-induced psoriasis-like skin inflammation.The Journal of clinical investigation · 2006Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Previously, a hypomorphic mutation in CD18 was generated by gene targeting, with homozygous mice displaying increased circulating neutrophil counts, defects in the response to chemically induced peritonitis, and delays in transplantation rejection. When this mutation was backcrossed onto the PL/J inbred strain, virtually all homozygous mice developed a chronic inflammatory skin disease with a mean age of onset of 11 weeks after birth. The disease was characterized by erythema, hair loss, and the development of scales and crusts. The histopathology revealed hyperplasia of the epidermis, subcorneal microabscesses, orthohyperkeratosis, parakeratosis, and lymphocyte exocytosis, which are features in common with human psoriasis and other hyperproliferative inflammatory skin disorders. Repetitive cultures failed to demonstrate bacterial or fungal organisms potentially involved in the pathogenesis of this disease, and the dermatitis resolved rapidly after subcutaneous administration of dexamethasone. Homozygous mutant mice on a (PL/J x C57BL/6J)F1 background did not develop the disease and backcross experiments suggest that a small number of genes (perhaps as few as one), in addition to CD18, determine susceptibility to the disorder. This phenotype provides a model for inflammatory skin disorders, may have general relevance to polygenic human inflammatory diseases, and should help to identify genes that interact with the beta2 integrins in inflammatory processes.
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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.