ReviewCurrent rheumatology reports1999
Genetic and immunologic features associated with scleroderma-like syndrome of TSK mice.
Review in Current rheumatology reports, 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
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
8 citing papers in PubMed, 24 citations in OpenAlex.
- Article
- B cells in systemic sclerosis: from pathophysiology to treatment.Clinical rheumatology · 2021Review
- Recent advances in the genetics of systemic sclerosis: toward biological and clinical significance.Current rheumatology reports · 2015Review
- B-cell depletion therapy in systemic sclerosis: experimental rationale and update on clinical evidence.International journal of rheumatology · 2011Article
- Molecular aspects of regulation of collagen gene expression in fibrosis.Journal of clinical immunology · 2005Review
- B Lymphocyte signaling established by the CD19/CD22 loop regulates autoimmunity in the tight-skin mouse.The American journal of pathology · 2004Article
- Animal models for scleroderma: an update.Current rheumatology reports · 2002Review
- Elevated expression of isopeptide bond cross-links contributes to fibrosis in scleroderma and the healing wounds of tight skin mice.Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair SocietyArticle
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
No grant is acknowledged in the PubMed record.
Abstract
Tight-skin (TSK) mouse, the experimental model for scleroderma, develops cutaneous hyperplasia and autoantibodies to scleroderma specific autoantigens. TSK syndrome is caused by a mutation on chromosome 2. Induction of cutaneous hyperplasia is due to intragenic duplication of exons 17 to 40 of fibrillin-1 gene, mapping close to TSK locus. The mutant mouse expresses a 14kb Fbn transcript in addition to 11kb wild-type transcript. Immunoprecipation analysis confirms that the mutant transcript is functional and codes for a 420kD fibrillin. The occurrence of TSK syndrome is independent of the presence of mature lymphocytes although splenic/bone marrow cells appear to be capable of transferring the disease in normal animals. Transgenic mice expressing mutant transgene develop mild skin thickness with associate biochemical changes but do not develop anti-topo I antibodies. Among the other factors that may contribute to the develop- ment of hyperplasia, collagen V seems to play an important role.
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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.