ArticleClinical and experimental immunology1999
A syndrome resembling human systemic sclerosis (scleroderma) in MRL/lpr mice lacking interferon-gamma (IFN-gamma) receptor (MRL/lprgammaR-/-).
Article in Clinical and experimental immunology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed, 31 citations in OpenAlex.
- Animal Models of Systemic Sclerosis: Using Nailfold Capillaroscopy as a Potential Tool to Evaluate Microcirculation and Microangiopathy: A Narrative Review.Life (Basel, Switzerland) · 2022Review
- Improving translational research in sex-specific effects of comorbidities and risk factors in ischaemic heart disease and cardioprotection: position paper and recommendations of the ESC Working Group on Cellular Biology of the Heart.Cardiovascular research · 2021Review
- Molecular pathogenesis of skin fibrosis: insight from animal models.Current rheumatology reports · 2010Review
- The role of B cells in systemic sclerosis.Biologics : targets & therapy · 2008Article
- Use of localised gene transfer to develop new treatment strategies for the salivary component of Sjögren's syndrome.Annals of the rheumatic diseases · 2003Review
- Animal models for scleroderma: an update.Current rheumatology reports · 2002Review
- Progress in systemic sclerosis: novel therapeutic paradigms.Current rheumatology reports · 2000Review
- T lymphocyte and fibroblast interactions: the case of skin involvement in systemic sclerosis and other examples.Springer seminars in immunopathology · 1999Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MRL/lpr mice develop a systemic autoimmune disease characterized by autoantibodies and inflammatory lesions in various organs. The main cause of early mortality is glomerulonephritis. We previously found that MRL/lprgammaR-/- mice are protected from glomerulonephritis and have an increased life span compared with their MRL/lprgammaR+/+ littermates. We now carried out a histopathological study of a selection of organs of MRL/lprgammaR-/- mice. Mice were killed as soon as they showed clinical signs of disease. In the majority of animals skin lesions were the first apparent pathology. Mononuclear cell infiltrates were frequent in skin, lungs and kidneys, and they occurred also in liver, salivary glands and heart. In infiltrated areas there was an abnormal accumulation of bundles of collagen. In the lungs of MRL/lprgammaR-/- mice, and occasionally in other organs, small and middle-sized arteries and veins showed intimal proliferation, resulting in a narrowed lumen. Alveolitis was widespread. Mononuclear cell infiltrates and excessive production of collagen in the skin and several visceral organs, thickening of vascular intima and autoantibodies are characteristic features of human systemic sclerosis. Thus, MRL/lprgammaR-/- mice might represent a model for that disease.
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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.