Evidence map›Paper›PMID 23099863›Full record

ArticleDiabetes2013

Nonviral-mediated hepatic expression of IGF-I increases Treg levels and suppresses autoimmune diabetes in mice.

Xavier M Anguela, Sabrina Tafuro, Carles Roca, David Callejas, Judith Agudo, Mercè Obach, Albert Ribera, Albert Ruzo, Christopher J Mann, Alba Casellas and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Diabetes, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.9field-weighted citation impact, top 13% 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

19 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Insulin/IGF-1 signaling promotes immunosuppression via the STAT3 pathway: impact on the aging process and age-related diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021
    Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. AAV-mediated pancreatic overexpression ofMolecular metabolism · 2017
    Article
  12. Frontiers in immunology · 2017
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. 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

11 authors at 2 institutions in 1 country.

Xavier M AnguelaCenter of Animal Biotechnology and Gene Therapy, Universitat Autònoma de Barcelona, Bellaterra, Spain.
Sabrina Tafuro
Carles Roca
David Callejas
Judith Agudo
Mercè Obach
Albert Ribera
Albert Ruzo
Christopher J Mann
Alba Casellas
Fatima Bosch
Universitat Autònoma de Barcelona · ESCentro de Investigación Biomédica en Red Diabetes y Enfermedades Metabólicas Asociadas · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In type 1 diabetes, loss of tolerance to β-cell antigens results in T-cell-dependent autoimmune destruction of β cells. The abrogation of autoreactive T-cell responses is a prerequisite to achieve long-lasting correction of the disease. The liver has unique immunomodulatory properties and hepatic gene transfer results in tolerance induction and suppression of autoimmune diseases, in part by regulatory T-cell (Treg) activation. Hence, the liver could be manipulated to treat or prevent diabetes onset through expression of key genes. IGF-I may be an immunomodulatory candidate because it prevents autoimmune diabetes when expressed in β cells or subcutaneously injected. Here, we demonstrate that transient, plasmid-derived IGF-I expression in mouse liver suppressed autoimmune diabetes progression. Suppression was associated with decreased islet inflammation and β-cell apoptosis, increased β-cell replication, and normalized β-cell mass. Permanent protection depended on exogenous IGF-I expression in liver nonparenchymal cells and was associated with increased percentage of intrapancreatic Tregs. Importantly, Treg depletion completely abolished IGF-I-mediated protection confirming the therapeutic potential of these cells in autoimmune diabetes. This study demonstrates that a nonviral gene therapy combining the immunological properties of the liver and IGF-I could be beneficial in the treatment of the disease.

Indexed as

Genetic TherapyAnimalsApoptosisCell DivisionDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 1HumansInsulin-Like Growth Factor IInsulin-Secreting CellsLiverMiceMice, TransgenicPancreatitisPlasmidsT-Lymphocytes, RegulatoryInsulin-Like Growth Factor I

Identifiers

PMID23099863
PMCPMC3554392
OpenAlexW2146143116

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.