ReviewArthritis research & therapy2005
Aetiology and pathogenesis of reactive arthritis: role of non-antigen-presenting effects of HLA-B27.
Review in Arthritis research & therapy, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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.
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Who cites it
7 citing papers in PubMed, 25 citations in OpenAlex.
- Modulation of TNF-α, IL-1β and myeloperoxidase contributes to the anti-inflammatory and analgesic effects of Paullinia pinnata Linn (Sapindaceae) extracts in complete Freund's adjuvant-induced mono-arthritis in rats.Journal of ethnopharmacology · 2026Article
- Immunologic derangement caused by intestinal dysbiosis and stress is the intrinsic basis of reactive arthritis.Zeitschrift fur Rheumatologie · 2024Review
- Phosphorylation of STAT-1 serine 727 is prolonged in HLA-B27-expressing human monocytic cells.PloS one · 2013Article
- Enhanced phosphorylation of STAT-1 is dependent on double-stranded RNA-dependent protein kinase signaling in HLA-B27-expressing U937 monocytic cells.Arthritis and rheumatism · 2012Article
- Altered PKR Signalling and C / EBPβ Expression is Associated with HLA-B27 Expression in Monocytic Cells.Scandinavian journal of immunology · 2012Article
- Article
- Distribution of HLA-B27 and its alleles in patients with reactive arthritis and with ankylosing spondylitis in Tunisia.Rheumatology international · 2009Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Spondyloarthropathies are inflammatory diseases closely associated with human leukocyte antigen (HLA)-B27 by unknown mechanisms. One of these diseases is reactive arthritis (ReA), which is typically triggered by Gram-negative bacteria, which have lipopolysaccharide as an integral component of their outer membrane. Several findings in vivo and in vitro obtained from patients with ReA and from different model systems suggest that HLA-B27 modulates the interaction between ReA-triggering bacteria and immune cells by a mechanism unrelated to the antigen presentation function of HLA-B27. In this review we piece together a jigsaw puzzle from the new information obtained from the non-antigen-presenting effects of HLA-B27.
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.