Evidence map›Paper›PMID 11564376›Full record

ReviewCurrent rheumatology reports2001

Pathways of cell activation in spondyloarthropathies.

U Fearon, D J Veale

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current rheumatology reports, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact, top 90% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed, 5 citations in OpenAlex.

  1. Review
  2. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

U FearonThe Department of Rheumatology, St. Vincent's University Hospital, Elm Park, Dublin 4, Ireland.
D J Veale
St. Vincent's University Hospital · IE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The initiating event in cell activation is unknown in most autoimmune diseases. The role of infection is clear in some cases, especially in reactive arthritis; however, there is little evidence of a specific organism in other spondyloarthropathies. Common pathways of cell-cell interaction and activation manifest in inflammation, but subtle differences may exist. The presence of T cells, macrophages, and B-lymphocytes suggest an autoimmune mechanism; the arthritogenic peptide theory has been proposed. Furthermore, the association of spondyloarthropathies with HLA-B27 suggests it may be important in synovial T-cell activation. Other cell types involved in the process of bone and cartilage destruction, including fibroblasts and osteoclasts, may also be activated. Endothelial activation and angiogenesis may be a critical primary event in these diseases. Finally, trauma (physical or psychological) in the form of stress may be an important factor; the nervous system and neuropeptides may play a role in cell activation and initiation of arthritis.

Indexed as

Cell DivisionDisease ProgressionEndothelium, VascularHumansMacrophagesNeovascularization, PathologicOsteocytesPrognosisRisk AssessmentRisk FactorsSeverity of Illness IndexSpineSpondylarthropathies

Identifiers

PMID11564376
OpenAlexW2026447499

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.