Evidence map›Paper›PMID 24405551›Full record

ArticleArthritis research & therapy2014

Characterization of T cell phenotype and function in a double transgenic (collagen-specific TCR/HLA-DR1) humanized model of arthritis.

Bo Tang, Seunghyun Kim, Sarah Hammond, David L Cullins, David D Brand, Edward F Rosloniec, John M Stuart, Arnold E Postlethwaite, Andrew H Kang, Linda K Myers

Open access · goldAbstract read
In one paragraph

Article in Arthritis research & therapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.1field-weighted citation impact, top 21% 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

11 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
  2. Article
  3. CD8Journal of immunology (Baltimore, Md. : 1950) · 2022
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. The role of Syk in peripheral T cells.Clinical immunology (Orlando, Fla.) · 2018
    Article
  10. Article
  11. 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

10 authors at 1 institution in 1 country.

Bo Tang
Seunghyun Kim
Sarah Hammond
David L Cullins
David D Brand
Edward F Rosloniec
John M Stuart
Arnold E Postlethwaite
Andrew H Kang
Linda K Myers
University of Tennessee Health Science Center · US

Funding

Immune Suppression of Collagen ArthritisR01AR055661 · NIAMS · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI MYERS, LINDA K. · 2009 to 2013
$2.1M
20(OH) Vit D3, T Cells, and ArthritisR01AR064825 · NIAMS · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI KANG, ANDREW H · 2014 to 2018
$1.6M
Suppression of Collagen Induced Arthritis with Altered Peptide LigandsR01AR055266 · NIAMS · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI KANG, ANDREW H · 2009 to 2010
$740k
NIAMS NIH HHS AR-55266NIAMS NIH HHS AR-55661NIAMS NIH HHS R01 AR064825
6 · The paper itself

Abstract

introductionT cells orchestrate joint inflammation in rheumatoid arthritis (RA), yet they are difficult to study due to the small numbers of antigen-specific cells. The goal of this study was to characterize a new humanized model of autoimmune arthritis and to describe the phenotypic and functional changes that occur in autoimmune T cells following the induction of pathological events.

methodsWe developed a double transgenic mouse containing both the HLA-DR1 transgene and an HLA-DR1-restricted collagen-specific TCR in order to obtain large numbers of antigen-specific T cells that can be used for immunologic studies.

resultsIn vitro, CII-specific T cells from this mouse proliferated vigorously in response to the CII immunodominant peptide A2 and the cells altered their phenotype to become predominately CD62Llow and CD44high "activated" T cells. The response was accompanied by the production of Th1, Th2, and Th17-type cytokines. Following immunization with bovine CII/CFA, these mice develop an accelerated arthritis compared to single transgenic HLA-DR1 mice. On the other hand, when the mice were treated orally with the analog peptide A12, (a suppressive analog of collagen we have previously described), arthritis was significantly suppressed, despite the fact that >90% of the CD4+ T cells express the TCR Tg. In GALT tissues taken from the A12-treated mice, IL-2, IFN-γ, and IL-17 production to the autoimmune collagen determinant dropped while high levels of IL-10 and IL-4 were produced.

conclusionsWe have developed a humanized model of autoimmune arthritis that will be useful for the study of T cell directed therapies as well as T cell mediated mechanisms of autoimmune diseases.

Indexed as

Adoptive TransferAnimalsArthritis, ExperimentalArthritis, RheumatoidCytokinesFlow CytometryHLA-DR1 AntigenHumansImmunophenotypingMiceMice, TransgenicPhenotypeReceptors, Antigen, T-CellT-LymphocytesCytokinesHLA-DR1 AntigenReceptors, Antigen, T-Cell

Identifiers

PMID24405551
PMCPMC3978884
OpenAlexW2153888492

What OpenQuestion holds

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LicenceCC BY
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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.