ReviewCurrent rheumatology reports2006
Pathogenesis of spondyloarthritis: insights from synovial membrane studies.
Review in Current rheumatology reports, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed, 11 citations in OpenAlex.
- Synovitis in spondyloarthritides.The open rheumatology journal · 2011Article
- Interactions of the innate and adaptive arms of the immune system in the pathogenesis of spondyloarthritis.Clinical and experimental rheumatologyReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Here, we review histopathologic studies of the cellular and molecular pathways of spondyloarthritis (SpA) synovial inflammation. In contrast with lymphocytes, specific macrophage subsets and polymorphonuclear cells selectively increase in SpA synovitis, correlate with global disease activity, decrease rapidly upon effective treatment with tumor necrosis factor (TNF)-alpha blockers, and serve as valuable biomarkers for treatment response in SpA. Functionally, increased Toll-like receptor triggering may be responsible for the proinflammatory response of these cells. Therefore, we propose that an exaggerated response of the innate immune system in genetically susceptible patients rather than a classic, lymphocyte-mediated autoimmune process is involved in the pathogenesis of SpA.
Indexed as
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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.