Evidence map›Paper›PMID 29259578›Full record

ReviewFrontiers in endocrinology2017

T Cell-Mediated Beta Cell Destruction: Autoimmunity and Alloimmunity in the Context of Type 1 Diabetes.

Adam L Burrack, Tijana Martinov, Brian T Fife

Abstract readReview
In one paragraph

Review in Frontiers in endocrinology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 170 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
170citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

170 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
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  16. Extracellular vesicles fromFrontiers in immunology · 2026
    Article
  17. Article
  18. 3D Bioprinting Strategies in Autoimmune Disease Models.International journal of molecular sciences · 2025
    Review
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  20. Review

110 more citing papers are in PubMed but not listed here.

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.

Adam L BurrackDepartment of Medicine, Center for Immunology, University of Minnesota Medical School, Minneapolis, MN, United States.
Tijana MartinovDepartment of Medicine, Center for Immunology, University of Minnesota Medical School, Minneapolis, MN, United States.
Brian T FifeDepartment of Medicine, Center for Immunology, University of Minnesota Medical School, Minneapolis, MN, United States.

Funding

Type I interferons in tolerance in the steady stateP01AI035296 · NIAID · UNIVERSITY OF MINNESOTA TWIN CITIES · PI MUELLER, DANIEL L · 1993 to 2023
$31.1M
TRAINING GRANT IN DIABETES, ENDOCRINOLOGY, &METABOLISMT32DK007203 · NIDDK · UNIVERSITY OF MINNESOTA TWIN CITIES · PI LISA Senye CHOW, Douglas G Mashek · 1986 to 2026
$4.3M
Multiplex immune analysis of antigen specific CD4+ T cells in autoimmune diabetesU24AI118635 · NIAID · UNIVERSITY OF MINNESOTA · PI FIFE, BRIAN T · 2015 to 2019
$2.3M
Mechanisms of immune tolerance in autoimmune diabetesR01AI106791 · NIAID · UNIVERSITY OF MINNESOTA · PI FIFE, BRIAN T · 2014 to 2018
$1.9M
NIAID NIH HHS P01 AI035296NIAID NIH HHS R01 AI106791NIAID NIH HHS U24 AI118635NIDDK NIH HHS T32 DK007203
6 · The paper itself

Abstract

Type 1 diabetes (T1D) results from destruction of pancreatic beta cells by T cells of the immune system. Despite improvements in insulin analogs and continuous blood glucose level monitoring, there is no cure for T1D, and some individuals develop life-threatening complications. Pancreas and islet transplantation have been attractive therapeutic approaches; however, transplants containing insulin-producing cells are vulnerable to both recurrent autoimmunity and conventional allograft rejection. Current immune suppression treatments subdue the immune system, but not without complications. Ideally a successful approach would target only the destructive immune cells and leave the remaining immune system intact to fight foreign pathogens. This review discusses the autoimmune diabetes disease process, diabetic complications that warrant a transplant, and alloimmunity. First, we describe the current understanding of autoimmune destruction of beta cells including the roles of CD4 and CD8 T cells and several possibilities for antigen-specific tolerance induction. Second, we outline diabetic complications necessitating beta cell replacement. Third, we discuss transplant recognition, potential sources for beta cell replacement, and tolerance-promoting therapies under development. We hypothesize that a better understanding of autoreactive T cell targets during disease pathogenesis and alloimmunity following transplant destruction could enhance attempts to re-establish tolerance to beta cells.

Indexed as

alloimmunityautoimmune diseasesimmunologyT cellstolerance inductiontransplantation immunologytype 1 diabetes

Identifiers

PMID29259578
PMCPMC5723426

What OpenQuestion holds

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Registered trials

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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.