Evidence map›Paper›PMID 21305522›Full record

ArticleArthritis and rheumatism2011

Proteoglycan-induced arthritis and recombinant human proteoglycan aggrecan G1 domain-induced arthritis in BALB/c mice resembling two subtypes of rheumatoid arthritis.

Tibor T Glant, Marianna Radacs, Gyorgy Nagyeri, Katalin Olasz, Anna Laszlo, Ferenc Boldizsar, Akos Hegyi, Alison Finnegan, Katalin Mikecz

Open access · greenAbstract read
In one paragraph

Article in Arthritis and rheumatism, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
6.0field-weighted citation impact, top 4% 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

45 citing papers in PubMed, 69 citations in OpenAlex.

  1. Article
  2. Proteasome Inhibitors: Potential in Rheumatoid Arthritis Therapy?International journal of molecular sciences · 2025
    Review
  3. Article
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  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Ameliorated Autoimmune Arthritis and Impaired B Cell Receptor-Mediated CaInternational journal of molecular sciences · 2020
    Article
  15. Article
  16. DNA Methylation-Governed Gene Expression in Autoimmune Arthritis.International journal of molecular sciences · 2019
    Review
  17. Article
  18. Article
  19. Article
  20. Why Don't We Have a Vaccine Against Autoimmune Diseases? - A Review.Journal of clinical & cellular immunology · 2019
    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

9 authors at 1 institution in 1 country.

Tibor T GlantRush University Medical Center, Chicago, Illinois. Tibor_Glant@rsh.net
Marianna Radacs
Gyorgy Nagyeri
Katalin Olasz
Anna Laszlo
Ferenc Boldizsar
Akos Hegyi
Alison Finnegan
Katalin Mikecz
Rush University Medical Center · US

Funding

MAPPING OF ARTHRITIS SUSCEPTIBLE GENESP01AR045652 · NIAMS · RUSH UNIVERSITY MEDICAL CENTER · PI FINNEGAN, ALISON · 1999 to 2008
$9.4M
AUTOIMMUNE PROGRESSIVE POLYARTHRITISR01AR040310 · NIAMS · RUSH UNIVERSITY MEDICAL CENTER · PI GLANT, TIBOR T. · 1990 to 2009
$3.1M
B CELL FUNCTION IN AUTOIMMUNE ARTHRITISR01AR047657 · NIAMS · RUSH UNIVERSITY MEDICAL CENTER · PI FINNEGAN, ALISON · 2002 to 2011
$3.0M
Mapping of Arthritis Susceptibility GenesR01AR059356 · NIAMS · RUSH UNIVERSITY MEDICAL CENTER · PI GLANT, TIBOR T. · 2010 to 2014
$2.2M
MECHANISMS OF ARTHRITIS SUPPRESSION BY TSG-6 (TNFIP6)R01AR051163 · NIAMS · RUSH UNIVERSITY MEDICAL CENTER · PI MIKECZ, KATALIN · 2004 to 2008
$1.4M
NIAMS NIH HHS AR-040310NIAMS NIH HHS AR-045652NIAMS NIH HHS AR-047657NIAMS NIH HHS AR-051163NIAMS NIH HHS P01 AR045652NIAMS NIH HHS R01 AR040310NIAMS NIH HHS R01 AR047657NIAMS NIH HHS R01 AR051163NIAMS NIH HHS R01 AR059356
6 · The paper itself

Abstract

objectiveTo develop a simplified and relatively inexpensive version of cartilage proteoglycan-induced arthritis (PGIA), an autoimmunity model of rheumatoid arthritis (RA), and to evaluate the extent to which this new model replicates the disease parameters of PGIA and RA.

methodsRecombinant human G1 domain of human cartilage PG containing "arthritogenic" T cell epitopes was generated in a mammalian expression system and used for immunization of BALB/c mice. The development and progression of arthritis in recombinant human PG G1-immunized mice (designated recombinant human PG G1-induced arthritis [GIA]) was monitored, and disease parameters were compared with those in the parent PGIA model.

resultsGIA strongly resembled PGIA, although the clinical symptoms and immune responses in mice with GIA were more uniform than in those with PGIA. Mice with GIA showed evidence of stronger Th1 and Th17 polarization than those with PGIA, and anti-mouse PG autoantibodies were produced in different isotype ratios in the 2 models. Rheumatoid factor (RF) and anti-cyclic citrullinated peptide (anti-CCP) antibodies were detected in both models; however, serum levels of IgG-RF and anti-CCP antibodies were different in GIA and PGIA, and both parameters correlated better with disease severity in GIA than in PGIA.

conclusionGIA is a novel model of seropositive RA that exhibits all of the characteristics of PGIA. Although the clinical phenotypes are similar, GIA and PGIA are characterized by different autoantibody profiles, and the 2 models may represent 2 subtypes of seropositive RA, in which more than 1 type of autoantibody can be used to monitor disease severity and response to treatment.

Indexed as

AggrecansAnalysis of VarianceAnimalsArthritis, ExperimentalArthritis, RheumatoidCartilage, ArticularDisease Models, AnimalEnzyme-Linked Immunosorbent AssayFemaleImmunizationInterleukinsMiceMice, Inbred BALB CProteoglycansRheumatoid FactorT-LymphocytesAggrecansInterleukinsProteoglycansRheumatoid Factor

Identifiers

PMID21305522
PMCPMC3086933
OpenAlexW1978207888

What OpenQuestion holds

Textmetadata
LicenceTDM
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.