ReviewClinical rheumatology1996
Experimental spondyloarthropathy in HLA-B27 transgenic rats.
Review in Clinical rheumatology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 25 citations in OpenAlex.
- The 60Rheumatology and immunology research · 2026Article
- HLA-C*07 in axial spondyloarthritis: data from the German Spondyloarthritis Inception Cohort and the Spondyloarthritis Caught Early cohort.Genes and immunity · 2019Article
- IgA-coatedScience translational medicine · 2017Article
- Major histocompatibility complex associations of ankylosing spondylitis are complex and involve further epistasis with ERAP1.Nature communications · 2015Article
- Expression of HLA-B27 causes loss of migratory dendritic cells in a rat model of spondylarthritis.Arthritis and rheumatism · 2012Article
- Seronegative spondyloarthropathies: to lump or split?Annals of the rheumatic diseases · 2005Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rats of the LEW, F344, and PVG strains bearing high copy numbers of transgenes for HLA-B27 and human beta 2-microglobulin develop a multisystem disorder, many features of which resemble aspects of the human spondyloarthropathies, most dramatically axial and peripheral arthropathy. The disease is not seen in rats with comparable expression of HLA-B7, and so is relatively specific for HLA-B27. It requires T cells and another bone marrow derived cell, as well as an intact gut flora. Characteristic cytokine profiles distinguish the inflammatory infiltrates in the gut and the joint, and the earliest T cell infiltrates at these sites are polyclonal. Polymorphism at the Tap-2 peptide transporter locus has no significant effect on disease, whereas the DA strain background abrogates disease. The molecular role of the B27 molecule in disease remains to be elucidated, but there is good reason to believe that it will eventually yield to continued investigation of this animal model.
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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.