Evidence map›Paper›PMID 20696780›Full record

ArticleThe American journal of pathology2010

Characterization of the KRN cell transfer model of rheumatoid arthritis (KRN-CTM), a chronic yet synchronized version of the K/BxN mouse.

Timothy P LaBranche, Cynthia L Hickman-Brecks, Debra M Meyer, Chad E Storer, Michael I Jesson, Kimberly M Shevlin, Fernando A Happa, Ruteja A Barve, David J Weiss, John C Minnerly and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

21 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
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  4. Review
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  15. IDO2: A Pathogenic Mediator of Inflammatory Autoimmunity.Clinical medicine insights. Pathology · 2016
    Review
  16. Review
  17. Article
  18. Article
  19. The cellular source and target of IL-21 in K/BxN autoimmune arthritis.Journal of immunology (Baltimore, Md. : 1950) · 2013
    Article
  20. Modulation of innate and adaptive immune responses by tofacitinib (CP-690,550).Journal of immunology (Baltimore, Md. : 1950) · 2011
    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

12 authors at 2 institutions in 1 country.

Timothy P LaBrancheGlobal Research & Development, Pfizer Inc., Chesterfield, Missouri, USA. timothy.labranche@pfizer.com
Cynthia L Hickman-Brecks
Debra M Meyer
Chad E Storer
Michael I Jesson
Kimberly M Shevlin
Fernando A Happa
Ruteja A Barve
David J Weiss
John C Minnerly
Jennifer L Racz
Paul M Allen
Pfizer (United States) · USWashington University in St. Louis · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In this study, a chronic yet synchronized version of the K/BxN mouse, the KRN-cell transfer model (KRN-CTM), was developed and extensively characterized. The transfer of purified splenic KRN T cells into T cell-deficient B6.TCR.Calpha(-/-)H-2(b/g7) mice induced anti-glucose 6-phosphate isomerase antibody-dependent chronic arthritis in 100% of the mice with uniform onset of disease 7 days after T cell transfer. Cellular infiltrations were assessed by whole-ankle transcript microarray, cytokine and chemokine levels, and microscopic and immunohistochemical analyses 7 through 42 days after T cell transfer. Transcripts identified an influx of monocytes/macrophages and neutrophils into the ankles and identified temporal progression of cartilage damage and bone resorption. In both serum and ankle tissue there was a significant elevation in interleukin-6, whereas macrophage inflammatory protein-1 alpha and monocyte chemotactic protein-1 were only elevated in tissue. Microscopic and immunohistochemical analyses revealed a time course for edema, synovial hypertrophy and hyperplasia, infiltration of F4/80-positive monocytes/macrophages and myeloperoxidase-positive neutrophils, destruction of articular cartilage, pannus invasion, bone resorption, extra-articular fibroplasia, and joint ankylosis. The KRN cell transfer model replicates many features of chronic rheumatoid arthritis in humans in a synchronized manner and lends itself to manipulation of adoptively transferred T cells and characterizing specific genes and T cell subsets responsible for rheumatoid arthritis pathogenesis and progression.

Indexed as

Disease Models, AnimalAnimalsArthritis, RheumatoidDisease ProgressionEnzyme-Linked Immunosorbent AssayFlow CytometryImmunohistochemistryInflammationJointsMacrophagesMiceMice, TransgenicMonocytesT-Lymphocytes

Identifiers

PMID20696780
PMCPMC2928971
OpenAlexW2119978797

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.