Evidence map›Paper›PMID 26039878›Full record

ArticlePloS one2015

Use of autoantigen-loaded phosphatidylserine-liposomes to arrest autoimmunity in type 1 diabetes.

Irma Pujol-Autonell, Arnau Serracant-Prat, Mary Cano-Sarabia, Rosa M Ampudia, Silvia Rodriguez-Fernandez, Alex Sanchez, Cristina Izquierdo, Thomas Stratmann, Manuel Puig-Domingo, Daniel Maspoch and 2 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

49 citing papers in PubMed, 89 citations in OpenAlex.

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  15. Emerging strategies for nanomedicine in autoimmunity.Advanced drug delivery reviews · 2024
    Review
  16. Review
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  18. Article
  19. Nanomaterials for antigen-specific immune tolerance therapy.Drug delivery and translational research · 2023
    Review
  20. Biomaterial Strategies for Selective Immune Tolerance: Advances and Gaps.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023
    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

12 authors at 6 institutions in 1 country.

Irma Pujol-AutonellImmunology Department, Germans Trias i Pujol Research Institute, Autonomous University of Barcelona, Badalona, Spain.
Arnau Serracant-PratImmunology Department, Germans Trias i Pujol Research Institute, Autonomous University of Barcelona, Badalona, Spain.
Mary Cano-SarabiaCatalan Institute of Nanoscience and Nanotechnology, Bellaterra, Spain.
Rosa M AmpudiaImmunology Department, Germans Trias i Pujol Research Institute, Autonomous University of Barcelona, Badalona, Spain.
Silvia Rodriguez-FernandezImmunology Department, Germans Trias i Pujol Research Institute, Autonomous University of Barcelona, Badalona, Spain.
Alex SanchezStatistics Department, Faculty of Biology, University of Barcelona, Barcelona, Spain.
Cristina IzquierdoDepartment of Physiology and Immunology, Faculty of Biology, University of Barcelona, Barcelona, Spain.
Thomas StratmannDepartment of Physiology and Immunology, Faculty of Biology, University of Barcelona, Barcelona, Spain.
Manuel Puig-DomingoEndocrinology and Nutrition Service, Hospital Germans Trias i Pujol, Badalona, Spain.
Daniel MaspochCatalan Institute of Nanoscience and Nanotechnology, Bellaterra, Spain; Institucio Catalana de Recerca i Estudis Avançats (ICREA), Barcelona, Spain.
Joan VerdaguerImmunology Unit, Department of Experimental Medicine, University of Lleida and IRBLleida, Lleida, Spain.
Marta Vives-PiImmunology Department, Germans Trias i Pujol Research Institute, Autonomous University of Barcelona, Badalona, Spain.
Institut d'Investigació en Ciències de la Salut Germans Trias i Pujol · ESUniversitat de Barcelona · ESInstitut Català de Nanociència i Nanotecnologia · ESHospital Universitari Germans Trias i Pujol · ESUniversitat Autònoma de Barcelona · ESUniversitat de Lleida · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionThe development of new therapies to induce self-tolerance has been an important medical health challenge in type 1 diabetes. An ideal immunotherapy should inhibit the autoimmune attack, avoid systemic side effects and allow β-cell regeneration. Based on the immunomodulatory effects of apoptosis, we hypothesized that apoptotic mimicry can help to restore tolerance lost in autoimmune diabetes.

objectiveTo generate a synthetic antigen-specific immunotherapy based on apoptosis features to specifically reestablish tolerance to β-cells in type 1 diabetes.

methodsA central event on the surface of apoptotic cells is the exposure of phosphatidylserine, which provides the main signal for efferocytosis. Therefore, phosphatidylserine-liposomes loaded with insulin peptides were generated to simulate apoptotic cells recognition by antigen presenting cells. The effect of antigen-specific phosphatidylserine-liposomes in the reestablishment of peripheral tolerance was assessed in NOD mice, the spontaneous model of autoimmune diabetes. MHC class II-peptide tetramers were used to analyze the T cell specific response after treatment with phosphatidylserine-liposomes loaded with peptides.

resultsWe have shown that phosphatidylserine-liposomes loaded with insulin peptides induce tolerogenic dendritic cells and impair autoreactive T cell proliferation. When administered to NOD mice, liposome signal was detected in the pancreas and draining lymph nodes. This immunotherapy arrests the autoimmune aggression, reduces the severity of insulitis and prevents type 1 diabetes by apoptotic mimicry. MHC class II tetramer analysis showed that peptide-loaded phosphatidylserine-liposomes expand antigen-specific CD4+ T cells in vivo. The administration of phosphatidylserine-free liposomes emphasizes the importance of phosphatidylserine in the modulation of antigen-specific CD4+ T cell expansion.

conclusionsWe conclude that this innovative immunotherapy based on the use of liposomes constitutes a promising strategy for autoimmune diseases.

Indexed as

AutoimmunityAnimalsAutoantigensCD4-Positive T-LymphocytesCell DifferentiationCytokinesDendritic CellsDiabetes Mellitus, Type 1ImmunotherapyInjections, IntraperitonealInsulinLiposomesMice, Inbred NODPhenotypePhosphatidylserinesAutoantigensCytokinesInsulinLiposomesPhosphatidylserines

Identifiers

PMID26039878
PMCPMC4454589
OpenAlexW2122233361

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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.