Evidence map›Paper›PMID 26602422›Full record

ArticleDiabetologia2016

Insulitis and characterisation of infiltrating T cells in surgical pancreatic tail resections from patients at onset of type 1 diabetes.

Lars Krogvold, Anna Wiberg, Bjørn Edwin, Trond Buanes, Frode Lars Jahnsen, Kristian F Hanssen, Erik Larsson, Olle Korsgren, Oskar Skog, Knut Dahl-Jørgensen

Open access · bronzeAbstract read
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In one paragraph

Article in Diabetologia, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
8.4field-weighted citation impact, top 2% 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

50 citing papers in PubMed, 93 citations in OpenAlex.

  1. TLR5 influences the development of type 1 diabetes.BMJ open diabetes research & care · 2025
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  19. One in Ten CD8Diabetes · 2021
    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

10 authors at 3 institutions in 2 countries.

Lars KrogvoldPaediatric Department, Oslo University Hospital HF, PO Box 4950, Nydalen, N-0424, Oslo, Norway. lars.krogvold@gmail.com.
Anna WibergDepartment of Immunology, Genetics and Pathology, Uppsala University, Uppsala, Sweden.
Bjørn EdwinFaculty of Medicine, University of Oslo, Oslo, Norway.
Trond BuanesFaculty of Medicine, University of Oslo, Oslo, Norway.
Frode Lars JahnsenDepartment of Pathology, Oslo University Hospital, Oslo, Norway.
Kristian F HanssenFaculty of Medicine, University of Oslo, Oslo, Norway.
Erik LarssonDepartment of Immunology, Genetics and Pathology, Uppsala University, Uppsala, Sweden.
Olle KorsgrenDepartment of Immunology, Genetics and Pathology, Uppsala University, Uppsala, Sweden.
Oskar SkogDepartment of Immunology, Genetics and Pathology, Uppsala University, Uppsala, Sweden.
Knut Dahl-JørgensenPaediatric Department, Oslo University Hospital HF, PO Box 4950, Nydalen, N-0424, Oslo, Norway.
Oslo University Hospital · NOUppsala University · SEUniversity of Oslo · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aims/hypothesisIt is thought that T cells play a major role in the immune-mediated destruction of beta cells in type 1 diabetes, causing inflammation of the islets of Langerhans (insulitis). The significance of insulitis at the onset of type 1 diabetes is debated, and the role of the T cells poorly understood.

methodsIn the Diabetes Virus Detection (DiViD) study, pancreatic tissue from six living patients with recent-onset type 1 diabetes was collected. The insulitis was characterised quantitatively by counting CD3(+) T cells, and qualitatively by transcriptome analysis targeting 84 T and B lymphocyte genes of laser-captured microdissected islets. The findings were compared with gene expression in T cells collected from kidney biopsies from allografts with ongoing cellular rejection. Cytokine and chemokine release from isolated islets was characterised and compared with that from islets from non-diabetic organ donors.

resultsAll six patients fulfilled the criteria for insulitis (5-58% of the insulin-containing islets in the six patients had ≥ 15 T cells/islet). Of all the islets, 36% contained insulin, with several resembling completely normal islets. The majority (61-83%) of T cells were found as peri-insulitis rather than within the islet parenchyma. The expression pattern of T cell genes was found to be markedly different in islets compared with the rejected kidneys. The islet-infiltrating T cells showed only background levels of cytokine/chemokine release in vitro. CONCLUSIONS/

interpretationInsulitis and a significant reserve reservoir for insulin production were present in all six cases of recent-onset type 1 diabetes. Furthermore, the expression patterns and levels of cytokines argue for a different role of the T cells in type 1 diabetes when compared with allograft rejection.

Indexed as

AdultB-Lymphocyte SubsetsDiabetes Mellitus, Type 1FemaleHumansInsulinMalePancreasT-LymphocytesYoung AdultInsulinGene expressionInflammationInsulinInsulitisPancreasT cellsType 1 diabetes

Identifiers

PMID26602422
OpenAlexW2178597235

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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.