Evidence map›Paper›PMID 9022077›Full record

ArticleThe Journal of clinical investigation1997

Inhibition of T cell apoptosis in the rheumatoid synovium.

M Salmon, D Scheel-Toellner, A P Huissoon, D Pilling, N Shamsadeen, H Hyde, A D D'Angeac, P A Bacon, P Emery, A N Akbar

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed, 1 pooled it
17.0field-weighted citation impact, top 1% 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

71 citing papers in PubMed, 1 synthesis or guideline pooled it, 472 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Network Pharmacology Study onInternational journal of molecular sciences · 2021
    Article
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  7. T Cells and Regulated Cell Death: Kill or Be Killed.International review of cell and molecular biology · 2019
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11 more citing papers are in PubMed but not listed here.

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

10 authors at 4 institutions in 2 countries.

M SalmonDepartment of Rheumatology, The University of Birmingham, United Kingdom.
D Scheel-Toellner
A P Huissoon
D Pilling
N Shamsadeen
H Hyde
A D D'Angeac
P A Bacon
P Emery
A N Akbar
University of Birmingham · GBCentre National de la Recherche Scientifique · FRThe Royal Free Hospital · GBUniversity College London · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Synovial T cells in rheumatoid arthritis are highly differentiated and express a phenotype suggesting susceptibility to apoptosis (CD45RB dull, CD45RO bright, Bcl-2 low, Bax high, Fas high). However, no evidence of T cell apoptosis was found in synovial fluid from any of 28 patients studied. In contrast, synovial fluid from 10 patients with crystal arthritis showed substantial levels of T cell apoptosis. The failre of apoptosis was not an intrinsic property of rheumatoid synovial T cells, as they showed rapid spontaneous apoptosis on removal from the joint. Synovial T cells from rheumatoid arthritis and gout patients could be rescued from spontaneous apoptosis in vitro either by IL-2R gamma chain signaling cytokines (which upregulate Bcl-2 and Bcl-XL) or by interaction with synovial fibroblasts (which upregulates Bcl-xL but not Bcl-2). The phenotype of rheumatoid synovial T cells ex vivo (Bcl-2 low, Bcl-xL high) suggested a fibroblast-mediated mechanism in vivo. This was confirmed by in vitro culture of synovial T cells with fibroblasts which maintained the Bcl-xL high Bcl-2 low phenotype. Synovial T cells from gout patients were Bcl-2 low Bcl-xL low and showed clear evidence of apoptosis in vivo. Inhibition experiments suggested that an integrin-ligand interaction incorporating the Arg-Gly-Asp motif is involved in fibroblast-mediated synovial T cell survival. We propose that environmental blockade of cell death resulting from interaction with stromal cells is a major factor in the persistent T cell infiltration of chronically inflamed rheumatoid synovium.

Indexed as

Proto-Oncogene Proteins c-bcl-2ApoptosisArthritis, GoutyArthritis, Rheumatoidbcl-X ProteinCells, CulturedCell SurvivalCoculture TechniquesFibroblastsFlow CytometryGenes, bcl-2HumansIntegrinsLeukocyte Common AntigensLymphocyte ActivationProto-Oncogene ProteinsBCL2L1 protein, humanbcl-X ProteinIntegrinsLeukocyte Common AntigensProto-Oncogene ProteinsProto-Oncogene Proteins c-bcl-2Receptors, Interleukin-2

Identifiers

PMID9022077
PMCPMC507817
OpenAlexW2064976851

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.