ReviewClinical rheumatology2006
TNF-receptor-associated periodic syndrome (TRAPS): an autosomal dominant multisystem disorder.
Review in Clinical rheumatology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
4 citing papers in PubMed, 19 citations in OpenAlex.
- Innate and adaptive immune abnormalities underlying autoimmune diseases: the genetic connections.Science China. Life sciences · 2023Review
- Revisiting TNF Receptor-Associated Periodic Syndrome (TRAPS): Current Perspectives.International journal of molecular sciences · 2020Review
- Late-onset TNF receptor-associated periodic syndrome presenting as recurrent urticarial rash and lymph nodes.BMJ case reports · 2018Article
- History of primary immunodeficiency diseases in iran.Iranian journal of pediatrics · 2010Article
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
The TNF-receptor-associated periodic syndrome (TRAPS) is an autosomal dominant auto-inflammatory disorder, characterized by recurrent febrile attacks and localized inflammation. TRAPS is caused by mutations in the gene encoding the TNF Receptor Super Family 1A (TNFRSF1A) on chromosome 12p13. However, the incomplete penetrance and genetic heterogeneity have been reported in this syndrome. Although the ethnic diversity and clinical heterogeneity may propose the role of other genes in the pathogenesis of TRAPS, some low-penetrance TNFRSF1A variants contribute to atypical inflammatory responses in other autoimmune diseases. Furthermore, molecular studies on TRAPS and other auto-inflammatory disorders could be suggested to identify additional genes coding the molecules in the TNF signalling process.
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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.