ReviewJournal of the Royal College of Physicians of London
Lupus in the Fas lane?
Review in Journal of the Royal College of Physicians of London. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 10 citations in OpenAlex.
- Heat shock protein 90 inhibition by 17-DMAG lessens disease in the MRL/lpr mouse model of systemic lupus erythematosus.Cellular & molecular immunology · 2012Article
- The biology of reactive intermediates in systemic lupus erythematosus.Autoimmunity · 2010Review
- Horizons in Sjögren's syndrome genetics.Clinical reviews in allergy & immunology · 2007Review
- The biology of nitric oxide and other reactive intermediates in systemic lupus erythematosus.Clinical immunology (Orlando, Fla.) · 2006Review
- Nitric oxide induces apoptosis in spleen lymphocytes from MRL/lpr mice.Journal of investigative medicine : the official publication of the American Federation for Clinical Research · 2004Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fas is a 43 kDa glycoprotein molecule which is involved in inducing apoptosis in both B and T lymphocytes. In the murine MRL/Ipr-Ipr model of systemic lupus erythematosus (SLE), the lymphoproliferation (lpr) mutation results in defective transcription of the gene that codes for the Fas protein. MRL mice which carry the homozygous recessive Ipr mutation develop a severe early-onset genetically predetermined autoimmune syndrome characterised by high IgG and autoantibody levels and a diffuse proliferative immune complex-mediated glomerulonephritis. Interest in the importance of Fas in SLE has risen with the observation that 60% of human subjects with lupus have elevated levels of the soluble Fas receptor in their serum and that the abnormal presence of this molecule may protect lymphocytes from undergoing apoptosis. In this review the importance of Fas in autoimmune pathogenesis is discussed.
Indexed as
Identifiers
8748102PMC5401240W2416006367What 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.