Evidence map›Paper›PMID 19099086›Full record

ArticleThe review of diabetic studies : RDS2008

Incomplete Killing And Enhanced Activation of Islet-Reactive CD8+ T Cells by FasL-Expressing Dendritic Cells Limits Protection from Diabetes.

Mikael Maksimow, Catharina Alam, Arno Hänninen

Open access · bronzeAbstract read
In one paragraph

Article in The review of diabetic studies : RDS, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.2field-weighted citation impact, top 44% 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

1 citing paper in PubMed, 2 citations in OpenAlex.

  1. 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

3 authors at 1 institution in 1 country.

Mikael MaksimowDepartment of Medical Microbiology and Immunology, and MediCity Research Laboratory, University of Turku, Finland.
Catharina Alam
Arno Hänninen
University of Turku · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsAutologous dendritic cells (DC) are a promising tool for induction of cytotoxic CD8+ T cell immunity against tumors and chronic viral infections. When armed with the death-inducing Fas-ligand (FasL, CD195), DC attenuate delayed-type hypersensitivity reactions and allotransplant rejection by promoting activation-induced cell death in T cells. We investigated the possibility of using FasL-expressing DC to induce deletion of islet-reactive CD8+ T cells in vivo, and to prevent destruction of pancreatic islets in a model of autoimmune diabetes.

methodsDC, propagated from mouse bone marrow cells, were purified and made to express FasL and islet-antigen via plasmid transfection. CD8+ T cells (OT-I cells) recognizing the antigen, ovalbumin, were adoptively transferred to transgenic mice expressing ovalbumin in islets (RIP-OVA(lo) mice), and these mice were primed with ovalbumin. To test the potential of DC to prevent diabetes in this model, the mice were later intravenously vaccinated with the transfected DC.

resultsTransfected DC induced partial deletion of antigen-reactive CD8+ T cells in vivo and reduced the level of lymphocyte infiltration into pancreatic islets. Diabetes developed less frequently in vaccinated mice, but this effect was limited. Further in vitro analysis showed that FasL-expressing DC not only deleted many of the responding CD8+ T cells but also promoted the expansion of surviving cells and their IFN-gamma production.

conclusionsFasL-expressing DC can also have stimulatory effects on CD8+ T cells warranting further investigation into the optimal design of tolerance-promoting DC-vaccination to prevent autoimmune diabetes.

Identifiers

PMID19099086
PMCPMC2613269
OpenAlexW238082512

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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.