Evidence map›Paper›PMID 15743466›Full record

ArticleArthritis research & therapy2005

Gene expression profiling in murine autoimmune arthritis during the initiation and progression of joint inflammation.

Vyacheslav A Adarichev, Csaba Vermes, Anita Hanyecz, Katalin Mikecz, Eric G Bremer, Tibor T Glant

Open access · goldAbstract read
In one paragraph

Article 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 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

17 citing papers in PubMed, 37 citations in OpenAlex.

  1. Dissecting the Immune System through Gene Regulation.Advances in experimental medicine and biology · 2024
    Article
  2. Review
  3. Article
  4. Article
  5. Genetics of rheumatoid arthritis - a comprehensive review.Clinical reviews in allergy & immunology · 2013
    Review
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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

6 authors at 2 institutions in 1 country.

Vyacheslav A AdarichevSection of Biochemistry and Molecular Biology, Department of Orthopedic Surgery, Rush University Medical Center, Chicago, Illinois, USA.
Csaba Vermes
Anita Hanyecz
Katalin Mikecz
Eric G Bremer
Tibor T Glant
Rush University Medical Center · USNorthwestern Memorial Hospital · 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
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 AR40310NIAMS NIH HHS AR45652NIAMS NIH HHS AR51163NIAMS NIH HHS P01 AR045652NIAMS NIH HHS R01 AR040310NIAMS NIH HHS R01 AR051163
6 · The paper itself

Abstract

We present here an extensive study of differential gene expression in the initiation, acute and chronic phases of murine autoimmune arthritis with the use of high-density oligonucleotide arrays interrogating the entire mouse genome. Arthritis was induced in severe combined immunodeficient mice by using adoptive transfer of lymphocytes from proteoglycan-immunized arthritic BALB/c mice. In this unique system only proteoglycan-specific lymphocytes are transferred from arthritic mice into syngeneic immunodeficient recipients that lack adaptive immunity but have intact innate immunity on an identical (BALB/c) genetic background.Differential gene expression in response to donor lymphocytes that migrated into the joint can therefore be monitored in a precisely timed manner, even before the onset of inflammation. The initiation phase of adoptively transferred disease (several days before the onset of joint swelling) was characterized by differential expression of 37 genes, mostly related to chemokines, interferon-gamma and tumor necrosis factor-alpha signaling, and T cell functions. These were designated early arthritis 'signature' genes because they could distinguish between the naive and the pre-arthritic state. Acute joint inflammation was characterized by at least twofold overexpression of 256 genes and the downregulation of 21 genes, whereas in chronic arthritis a total of 418 genes with an equal proportion of upregulated and downregulated transcripts were expressed differentially. Hierarchical clustering and functional classification of inflammation-related and arthritis-related genes indicated that the most common biological activities were represented by genes encoding interleukins, chemokine receptors and ligands, and by those involved in antigen recognition and processing.

Indexed as

Gene Expression ProfilingAcute DiseaseAdoptive TransferAnimalsArthritis, ExperimentalAutoimmune DiseasesChemokinesChronic DiseaseDisease ProgressionFemaleGene Expression RegulationHumansInterferon-gammaLymphocyte ActivationMiceMice, Inbred BALB CChemokinesInterferon-gammaProteoglycansTumor Necrosis Factor-alpha

Identifiers

PMID15743466
PMCPMC1065315
OpenAlexW1565031267

What OpenQuestion holds

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LicenceCC BY
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.