Evidence map›Paper›PMID 37625134›Full record

ArticleDiabetes2023

Reversal of Experimental Autoimmune Diabetes With an sCD39/Anti-CD3 Treatment.

Carmen Fotino, R Damaris Molano, Moufida Ben Nasr, Oliver Umland, Christopher A Fraker, Ulisse Ulissi, Hari Baskar Balasubramanian, Maria Elena Lunati, Vera Usuelli, Andy Joe Seelam and 8 more

Open access · greenAbstract read
In one paragraph

Article in Diabetes, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
2.1field-weighted citation impact, top 15% 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

4 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Extraislet expression of islet antigen boosts T cell exhaustion to partially prevent autoimmune diabetes.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  3. Article
  4. 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

18 authors at 4 institutions in 2 countries.

Carmen FotinoCell Transplant Center, Diabetes Research Institute, University of Miami, Miami, FL.ORCID 0000-0002-2645-6546
R Damaris MolanoCell Transplant Center, Diabetes Research Institute, University of Miami, Miami, FL.
Moufida Ben NasrInternational Center for T1D, Pediatric Clinical Research Center "Romeo ed Enrica Invernizzi," Department of Biomedical and Clinical Science L. Sacco, University of Milan, Milan, Italy.
Oliver UmlandCell Transplant Center, Diabetes Research Institute, University of Miami, Miami, FL.
Christopher A FrakerCell Transplant Center, Diabetes Research Institute, University of Miami, Miami, FL.
Ulisse UlissiCell Transplant Center, Diabetes Research Institute, University of Miami, Miami, FL.
Hari Baskar BalasubramanianInternational Center for T1D, Pediatric Clinical Research Center "Romeo ed Enrica Invernizzi," Department of Biomedical and Clinical Science L. Sacco, University of Milan, Milan, Italy.
Maria Elena LunatiDivision of Endocrinology, Azienda Socio-Sanitaria Territoriale (ASST) Fatebenefratelli-Sacco, Milan, Italy.
Vera UsuelliInternational Center for T1D, Pediatric Clinical Research Center "Romeo ed Enrica Invernizzi," Department of Biomedical and Clinical Science L. Sacco, University of Milan, Milan, Italy.
Andy Joe SeelamInternational Center for T1D, Pediatric Clinical Research Center "Romeo ed Enrica Invernizzi," Department of Biomedical and Clinical Science L. Sacco, University of Milan, Milan, Italy.
Salma Ayman KhalefaInternational Center for T1D, Pediatric Clinical Research Center "Romeo ed Enrica Invernizzi," Department of Biomedical and Clinical Science L. Sacco, University of Milan, Milan, Italy.
Christian La SalaCell Transplant Center, Diabetes Research Institute, University of Miami, Miami, FL.
Jennifer GimenoCell Transplant Center, Diabetes Research Institute, University of Miami, Miami, FL.
Armando J MendezCell Transplant Center, Diabetes Research Institute, University of Miami, Miami, FL.
Camillo RicordiCell Transplant Center, Diabetes Research Institute, University of Miami, Miami, FL.
Allison L BayerCell Transplant Center, Diabetes Research Institute, University of Miami, Miami, FL.
Paolo FiorinaInternational Center for T1D, Pediatric Clinical Research Center "Romeo ed Enrica Invernizzi," Department of Biomedical and Clinical Science L. Sacco, University of Milan, Milan, Italy.ORCID 0000-0002-1093-7724
Antonello PileggiCell Transplant Center, Diabetes Research Institute, University of Miami, Miami, FL.ORCID 0000-0001-7819-2813
University of Miami · USUniversity of Milan · ITBoston Children's Hospital · USASST Fatebenefratelli Sacco · IT

Funding

Diabetes Research Institute FoundationFondazione Diabete Ricerca (FO.DI.RI) Società Italiana di Diabetologia (SID) fellowshipItalian Ministry of Health RF-2016-02362512
6 · The paper itself

Abstract

Extracellular (e)ATP, a potent proinflammatory molecule, is released by dying/damaged cells at the site of inflammation and is degraded by the membrane ectonucleotidases CD39 and CD73. In this study, we sought to unveil the role of eATP degradation in autoimmune diabetes. We then assessed the effect of soluble CD39 (sCD39) administration in prevention and reversal studies in NOD mice as well as in mechanistic studies. Our data showed that eATP levels were increased in hyperglycemic NOD mice compared with prediabetic NOD mice. CD39 and CD73 were found expressed by both α- and β-cells and by different subsets of T cells. Importantly, prediabetic NOD mice displayed increased frequencies of CD3+CD73+CD39+ cells within their pancreata, pancreatic lymph nodes, and spleens. The administration of sCD39 into prediabetic NOD mice reduced their eATP levels, abrogated the proliferation of CD4+- and CD8+-autoreactive T cells, and increased the frequency of regulatory T cells, while delaying the onset of T1D. Notably, concomitant administration of sCD39 and anti-CD3 showed a strong synergism in restoring normoglycemia in newly hyperglycemic NOD mice compared with monotherapy with anti-CD3 or with sCD39. The eATP/CD39 pathway plays an important role in the onset of T1D, and its targeting might represent a potential therapeutic strategy in T1D. ARTICLE HIGHLIGHTS:

Indexed as

Antigens, CDApyraseDiabetes Mellitus, Type 15'-NucleotidaseAdenosine TriphosphateAnimalsCD3 ComplexDiabetes Mellitus, ExperimentalFemaleInsulin-Secreting CellsMiceMice, Inbred NODT-Lymphocytes, Regulatory5'-NucleotidaseAdenosine TriphosphateAntigens, CDApyraseCD39 antigenCD3 Complex

Identifiers

PMID37625134
PMCPMC10588287
OpenAlexW4386157815

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.