Evidence map›Paper›PMID 26271890›Full record

ArticleJournal of theoretical biology2015

Continuum model of T-cell avidity: Understanding autoreactive and regulatory T-cell responses in type 1 diabetes.

Majid Jaberi-Douraki, Massimo Pietropaolo, Anmar Khadra

Abstract read
In one paragraph

Article in Journal of theoretical biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 2 pooled it
2.2field-weighted citation impact, top 12% 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

10 citing papers in PubMed, 2 syntheses or guidelines pooled it, 20 citations in OpenAlex.

  1. Pooled it
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  7. 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

3 authors at 2 institutions in 2 countries.

Majid Jaberi-DourakiDepartment of Physiology, McGill University, H3G 1Y6, Quebec, Montreal, Canada.
Massimo PietropaoloDivision of Diabetes, Endocrinology and Metabolism, Baylor College of Medicine, Houston 77030, Texas, USA.
Anmar KhadraDepartment of Physiology, McGill University, H3G 1Y6, Quebec, Montreal, Canada. Electronic address: anmar.khadra@mcgill.ca.
Baylor College of Medicine · USMcGill University · CA

Funding

IMPROVING PREDICTION OF IDDMR01DK053456 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI HERMAN, MARK A, REDONDO, MARIA JOSE · 1999 to 2021
$9.5M
EPIDEMIOLOGY OF ISLET CELL AUTOIMMUNITY IN NIDDMR01DK056200 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PIETROPAOLO, MASSIMO T · 2001 to 2009
$3.5M
Proteomics of Autoimmune Type 1 DiabetesR21DK073724 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PIETROPAOLO, MASSIMO T · 2005 to 2006
$410k
NIDDK NIH HHS R01 DK053456NIDDK NIH HHS R01 DK056200NIDDK NIH HHS R01DK53456NIDDK NIH HHS R01DK56200NIDDK NIH HHS R21 DK073724NIDDK NIH HHS R21DK073724
6 · The paper itself

Abstract

Type 1 diabetes (T1D) is an autoimmune disease that results from the destruction of insulin-secreting pancreatic β cells, leading to abolition of insulin secretion and onset of diabetes. Cytotoxic CD4(+) and CD8(+) T cells, activated by antigen presenting cells (APCs), are both implicated in disease onset and progression. Regulatory T cells (Tregs), on the other hand, play a leading role in regulating immunological tolerance and resistant homoeostasis in T1D by suppressing effector T cells (Teffs). Recent data indicates that after activation, conventional Teffs transiently produce interleukin IL-2, a cytokine that acts as a growth factor for both Teffs and Tregs. Tregs suppress Teffs through IL-2 deprivation, competition and Teff conversion into inducible Tregs (iTregs). To investigate the interactions of these components during T1D progression, a mathematical model of T-cell dynamics is developed as a predictor of β-cell loss, with the underlying hypothesis that avidity of Teffs and Tregs, i.e., the binding affinity of T-cell receptors to peptide-major histocompatibility complexes on host cells, is continuum. The model is used to infer a set of criteria that determines susceptibility to T1D in high risk subjects. Our findings show that diabetes onset is guided by the absence of Treg-to-Teff dominance at specific high avidities, rather than over the whole range of avidity, and that the lack of overall dominance of Teffs-to-Tregs over time is the underlying cause of the "honeymoon period", the remission phase observed in some T1D patients. The model also suggests that competition between Teffs and Tregs is more effective than Teff-induction into iTregs in suppressing Teffs, and that a prolonged full width at half maximum of IL-2 release is a necessary condition for curbing disease onset. Finally, the model provides a rationale for observing rapid and slow progressors of T1D based on modest heterogeneity in the kinetic parameters.

Indexed as

Antibody AffinityAutoimmunityDiabetes Mellitus, Type 1Disease ProgressionHumansImmune ToleranceModels, ImmunologicalT-Lymphocytes, RegulatoryT-Lymphocyte SubsetsAvidity-dependent dominanceHoneymoon periodImmunomodulationInter- and intra-clonal competitionMathematical model

Identifiers

PMID26271890
PMCPMC4567915
OpenAlexW1155846412

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.