Evidence map›Paper›PMID 31309537›Full record

ReviewClinical and experimental immunology2019

Islet-immune interactions in type 1 diabetes: the nexus of beta cell destruction.

L Peters, A Posgai, T M Brusko

Open access · bronzeAbstract readReview
In one paragraph

Review in Clinical and experimental immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

23 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Review
  14. Review
  15. Review
  16. Article
  17. Type 1 diabetes mellitus: much progress, many opportunities.The Journal of clinical investigation · 2021
    Review
  18. Natural killer cells in inflammatory autoimmune diseases.Clinical & translational immunology · 2021
    Review
  19. Article
  20. 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

3 authors at 1 institution in 1 country.

L PetersDepartment of Pathology, Immunology and Laboratory Medicine, University of Florida Diabetes Institute, Gainesville, FL, USA.
A PosgaiDepartment of Pathology, Immunology and Laboratory Medicine, University of Florida Diabetes Institute, Gainesville, FL, USA.
T M BruskoDepartment of Pathology, Immunology and Laboratory Medicine, University of Florida Diabetes Institute, Gainesville, FL, USA.ORCID 0000-0002-7878-0014
University of Florida · US

Funding

Project 3P01AI042288 · NIAID · UNIVERSITY OF FLORIDA · PI Todd Michael Brusko · 1997 to 2026
$32.9M
The CD226 costimulatory axis in type 1 diabetesR01DK106191 · NIDDK · UNIVERSITY OF FLORIDA · PI Todd Michael Brusko · 2016 to 2026
$4.4M
Genetic Regulation of Human Beta Cell DestructionUC4DK104194 · NIDDK · UNIVERSITY OF FLORIDA · PI MATHEWS, CLAYTON E · 2014 to 2014
$3.1M
Interdisciplinary Graduate Program in Type 1 Diabetes and Biomedical EngineeringT32DK108736 · NIDDK · UNIVERSITY OF FLORIDA · PI MARK A. ATKINSON, Benjamin George Keselowsky · 2017 to 2026
$1.9M
NIAID NIH HHS P01 AI042288NIDDK NIH HHS R01 DK106191NIDDK NIH HHS T32 DK108736NIDDK NIH HHS UC4 DK104194
6 · The paper itself

Abstract

Recent studies in Type 1 Diabetes (T1D) support an emerging model of disease pathogenesis that involves intrinsic β-cell fragility combined with defects in both innate and adaptive immune cell regulation. This combination of defects induces systematic changes leading to organ-level atrophy and dysfunction of both the endocrine and exocrine portions of the pancreas, ultimately culminating in insulin deficiency and β-cell destruction. In this review, we discuss the animal model data and human tissue studies that have informed our current understanding of the cross-talk that occurs between β-cells, the resident stroma, and immune cells that potentiate T1D. Specifically, we will review the cellular and molecular signatures emerging from studies on tissues derived from organ procurement programs, focusing on in situ defects occurring within the T1D islet microenvironment, many of which are not yet detectable by standard peripheral blood biomarkers. In addition to improved access to organ donor tissues, various methodological advances, including immune receptor repertoire sequencing and single-cell molecular profiling, are poised to improve our understanding of antigen-specific autoimmunity during disease development. Collectively, the knowledge gains from these studies at the islet-immune interface are enhancing our understanding of T1D heterogeneity, likely to be an essential component for instructing future efforts to develop targeted interventions to restore immune tolerance and preserve β-cell mass and function.

Indexed as

AnimalsAutoimmunityDiabetes Mellitus, Type 1HumansImmune ToleranceInsulinInsulin-Secreting CellsIslets of LangerhansPancreasInsulinautoimmunitydiabeteshumaninflammationislet

Identifiers

PMID31309537
PMCPMC6857082
OpenAlexW2962298555

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.