Evidence map›Paper›PMID 16030184›Full record

ArticleBlood2005

Functional avidity directs T-cell fate in autoreactive CD4+ T cells.

Roberto Mallone, Sharon A Kochik, Helena Reijonen, Bryan Carson, Steven F Ziegler, William W Kwok, Gerald T Nepom

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

38 citing papers in PubMed, 62 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
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  9. Article
  10. T cell avidity and tumor immunity: problems and solutions.Cancer microenvironment : official journal of the International Cancer Microenvironment Society · 2014
    Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Production of primary human CD4⁺ T cell lines and clones.Methods in molecular biology (Clifton, N.J.) · 2013
    Article
  17. The pathogenesis and natural history of type 1 diabetes.Cold Spring Harbor perspectives in medicine · 2012
    Review
  18. Article
  19. Article
  20. 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

7 authors at 2 institutions in 1 country.

Roberto MalloneBenaroya Research Institute at Virginia Mason, 1201 Ninth Ave, Seattle, WA 98101, USA.
Sharon A Kochik
Helena Reijonen
Bryan Carson
Steven F Ziegler
William W Kwok
Gerald T Nepom
Benaroya Research InstituteVirginia Mason Medical Center · US

Funding

PATHOGENESIS OF TYPE 1.5 DIABETES IN THE GENERAL POPULATIONP01DK053004 · NIDDK · UNIVERSITY OF WASHINGTON · PI HOOD, LEROY E · 1998 to 2007
$5.3M
NIDDK NIH HHS P01 DK053004NIDDK NIH HHS P01 DK 53004
6 · The paper itself

Abstract

Major histocompatibility complex class II tetramer staining and activation analysis identified 2 distinct types of antigen-specific CD4+ T cells in the peripheral blood of humans with type 1 (autoimmune) diabetes. T cells with low-avidity recognition of peptide-MHC ligands had low sensitivity to activation and inefficient activation-induced apoptosis. In contrast, high-avidity T cells were highly sensitive to antigen-induced cell death through apoptotic mechanisms, and both apoptosis-resistant high- and low-avidity T cells that survived prolonged tetramer treatment were rendered anergic to restimulation by antigen. In addition, however, apoptosis-resistant high-avidity T cells acquired regulatory features, being able to suppress both antigen-specific and nonspecific CD4+ T-cell responses. This suppression was contact-dependent and correlated with the down-regulation of HLA class II and costimulatory molecules on antigen-presenting cells, including B cells and dendritic cells. T cells face a variety of fates following antigen exposure, including the paradoxic maintenance of high-avidity autoreactive T cells in the peripheral circulation, perhaps due to this capability of acquiring anergic and suppressive properties. Regulation via down-modulation of antigen-presenting cell function, a form of cell-to-cell licensing for suppression, also offers possibilities for the application of peptide-MHC therapeutics.

Indexed as

ApoptosisLymphocyte ActivationAdolescentAntigen-Presenting CellsAntigensCD4-Positive T-LymphocytesCells, CulturedClonal AnergyFemaleHumansPhenotypeProtein BindingSubstrate SpecificityAntigens

Identifiers

PMID16030184
PMCPMC1895305
OpenAlexW1998368928

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.