Evidence map›Paper›PMID 26948997›Full record

ReviewJournal of autoimmunity2016

Obstacles and opportunities for targeting the effector T cell response in type 1 diabetes.

Jane H Buckner, Gerald T Nepom

Open access · greenAbstract readReview
In one paragraph

Review in Journal of autoimmunity, 2016. 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
3.6field-weighted citation impact, top 8% 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, 23 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Review
  5. Epitope-based precision immunotherapy of Type 1 diabetes.Human vaccines & immunotherapeutics · 2023
    Article
  6. Article
  7. Article
  8. Beta cell-specific CD8Nature immunology · 2020
    Article
  9. Article
  10. TNature reviews. Immunology · 2020
    Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Beyond Genetics: What Causes Type 1 Diabetes.Clinical reviews in allergy & immunology · 2017
    Review
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

2 authors at 1 institution in 1 country.

Jane H BucknerBenaroya Research Institute at Virginia Mason, The University of Washington School of Medicine, Seattle, WA, USA. Electronic address: jbuckner@benaroyaresearch.org.
Gerald T NepomBenaroya Research Institute at Virginia Mason, The University of Washington School of Medicine, Seattle, WA, USA.
University of Washington · US

Funding

Immune Tolerance Network UM1 2023 SupplementUM1AI109565 · NIAID · BENAROYA RESEARCH INST AT VIRGINIA MASON · PI Mark S Anderson, Jane Hoyt Buckner · 2014 to 2026
$451.6M
Investigating the role of IL-6 signaling in Teff resistance and T1D developmentDP3DK104466 · NIDDK · BENAROYA RESEARCH INST AT VIRGINIA MASON · PI BUCKNER, JANE HOYT · 2014 to 2014
$752k
NIAID NIH HHS UM1 AI109565NIDDK NIH HHS DP3 DK104466
6 · The paper itself

Abstract

Autoreactive lymphocytes display a programmed set of characteristic effector functions and phenotypic markers that, in combination with antigen-specific profiling, provide a detailed picture of the adaptive immune response in Type 1 diabetes (T1D). The CD4+ T cell effector compartment (referred to as "Teff" in this article) has been extensively analyzed, particularly because the HLA genes most strongly associated with T1D are MHC class II alleles that form restriction elements for CD4+ T cell recognition. This "guilt by association" can now be revisited in terms of specific immune mechanisms and specific forms of T cell recognition that are displayed by Teff found in subjects with T1D. In this review, we describe properties of Teff that correlate with T1D, and discuss several characteristics that advance our understanding of disease persistence and progression. Focusing on functional disease-associated immunological pathways within these Teff suggests a rationale for next-generation clinical trials with targeted interventions. Indeed, immune modulation therapies in T1D that do not address these properties of Teff are unlikely to achieve durable clinical response.

Indexed as

Adaptive ImmunityAnimalsAutoantigensAutoimmunityCD4-Positive T-LymphocytesCombined Modality TherapyDiabetes Mellitus, Type 1Genetic Predisposition to DiseaseHistocompatibility Antigens Class IIHumansImmune ToleranceImmunomodulationImmunotherapyIslets of LangerhansMolecular Targeted TherapySignal TransductionAutoantigensHistocompatibility Antigens Class IICD4 T cellGenetic susceptibilityImmunomodulationType 1 diabetes

Identifiers

PMID26948997
PMCPMC4903876
OpenAlexW2292816348

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.