Evidence map›Paper›PMID 15642150›Full record

ReviewArthritis research & therapy2005

The role and clinical implications of G6PI in experimental models of rheumatoid arthritis.

Thomas Kamradt, David Schubert

Open access · diamondAbstract readReview
In one paragraph

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 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

10 citing papers in PubMed, 25 citations in OpenAlex.

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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 2 institutions in 1 country.

Thomas KamradtInstitut für Immunologie, Klinikum der Friedrich-Schiller Universität Jena, Jena, Germany. Immunologie@med.uni-jena.de
David Schubert
Friedrich Schiller University Jena · DEGerman Rheumatism Research Centre · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The antigens that trigger the pathogenic immune response in rheumatoid arthritis (RA) remain unknown. Until recently it was assumed that either viral or microbial antigens, or joint-specific antigens were the target of arthritogenic T and B lymphocytes in RA. Consequently, murine models of arthritis are induced by immunization with either joint-specific antigens such as type II collagen or microbial products such as streptococcal cell wall. In the K/BxN T-cell receptor transgenic mouse model arthritis is caused by a systemic autoimmune response to the ubiquitously expressed glycolytic enzyme glucose-6-phosphate isomerase (G6PI). The autoreactive transgenic T cells recognize G6PI and provide help for the production of arthritogenic IgG antibodies against G6PI. More recently it was shown that G6PI immunization induces severe symmetrical peripheral polyarthritis in genetically unaltered DBA/I mice. In that model CD4+ T cells are necessary not only for the induction but also for the effector phase of arthritis. Here we review the pathomechanisms that lead from systemic autoreactivity to arthritis in these models, consider the relevance of anti-G6PI immune reactivity for RA, and discuss the insights into the pathogenesis of RA and possibly other autoimmune conditions that can be gained from these models.

Indexed as

AnimalsAntibody SpecificityArthritis, ExperimentalArthritis, RheumatoidAutoantibodiesAutoantigensAutoimmune DiseasesB-LymphocytesCD4-Positive T-LymphocytesCell WallCollagen Type IIComplement System ProteinsCrosses, GeneticGlucose-6-Phosphate IsomeraseHistocompatibility Antigens Class IIHumansAutoantibodiesAutoantigensCollagen Type IIComplement System ProteinsGlucose-6-Phosphate IsomeraseHistocompatibility Antigens Class III-Ak antigenImmunoglobulin GInterleukin-1Receptors, Antigen, T-Cell

Identifiers

PMID15642150
PMCPMC1064898
OpenAlexW1910056502

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.