ReviewZeitschrift fur Rheumatologie2008
[Concepts on the pathogenesis of juvenile idiopathic arthritis].
Review in Zeitschrift fur Rheumatologie, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed, 7 citations in OpenAlex.
- Article
- Serum biomarkers for the diagnosis and monitoring of chronic recurrent multifocal osteomyelitis (CRMO).Rheumatology international · 2016Article
- Abatacept in difficult-to-treat juvenile idiopathic arthritis.Biologics : targets & therapy · 2008Article
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
There are various explanations for the development of juvenile idiopathic arthritis (JIA).Gene changes in the immune system can predispose to JIA and regulation of the immune system is crucial in the pathogenesis. The adaptive, acquired immune system probably plays a central role. Thus, in the case of JIA a conspicuous population of highly activated T-cells can be found in the synovia. B-cells are also involved, as indicated by positive ANA titers in JIA patients. Regulatory T-cells (Tregs) attempt to prevent the expansion of autoreactive T-cells.However, the natural or the innate immune system also plays a role. Thus a disorder of the inflammasome could underlie the cause of JIA with systemic onset. The interaction between congenital and adaptive immune system shows that a distinct spatial and temporal separation between the two immune systems is becoming increasingly difficult. An infection- and virus-related immune reaction could also be the cause of JIA. Proinflammatory cytokines are of proven significance in pathogenesis in terms of how they are released under stress, for example. New genomic and proteomic techniques are able to produce individualized profiles for each patient and allow for increasingly fine separation between subtypes, thus improving therapeutic possibilities.
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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.