Evidence map›Paper›PMID 31557322›Full record

ArticleImmunology2019

Stimulator of interferon genes agonists attenuate type I diabetes progression in NOD mice.

Henrique Lemos, Eslam Mohamed, Lei Huang, Phillip R Chandler, Rong Ou, Rafal Pacholczyk, Andrew L Mellor

Open access · bronzeAbstract read
In one paragraph

Article in Immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

18 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
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  7. Intracellular Sensing of DNA in Autoinflammation and Autoimmunity.Arthritis & rheumatology (Hoboken, N.J.) · 2022
    Review
  8. Review
  9. Review
  10. Review
  11. Review
  12. Article
  13. Review
  14. STING Signaling and Sterile Inflammation.Frontiers in immunology · 2021
    Review
  15. Review
  16. Article
  17. Review
  18. 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

7 authors at 3 institutions in 2 countries.

Henrique LemosInstitute of Cellular Medicine, Faculty of Medical Sciences, Newcastle University, Newcastle-upon-Tyne, UK.
Eslam MohamedDepartment of Immunology, H. Lee Moffitt Cancer Center & Research Institute, Tampa, FL, USA.
Lei HuangInstitute of Cellular Medicine, Faculty of Medical Sciences, Newcastle University, Newcastle-upon-Tyne, UK.
Phillip R ChandlerBiochemistry and Molecular Biology, Georgia Cancer Center, Augusta University, Augusta, GA, USA.
Rong OuInstitute of Cellular Medicine, Faculty of Medical Sciences, Newcastle University, Newcastle-upon-Tyne, UK.
Rafal PacholczykBiochemistry and Molecular Biology, Georgia Cancer Center, Augusta University, Augusta, GA, USA.
Andrew L MellorInstitute of Cellular Medicine, Faculty of Medical Sciences, Newcastle University, Newcastle-upon-Tyne, UK.ORCID 0000-0002-9553-6160
Newcastle University · GBAugusta University Health · USMoffitt Cancer Center · US

Funding

Engineering DNA nanoparticles to create immune toleranceR01AI103347 · NIAID · AUGUSTA UNIVERSITY · PI MELLOR, ANDREW LEE · 2013 to 2016
$1.5M
CSR NIH HHS AI103347NIAID NIH HHS R01 AI103347
6 · The paper itself

Abstract

Reagents that activate the signaling adaptor stimulator of interferon genes (STING) suppress experimentally induced autoimmunity in murine models of multiple sclerosis and arthritis. In this study, we evaluated STING agonists as potential reagents to inhibit spontaneous autoimmune type I diabetes (T1D) onset in non-obese diabetic (NOD) female mice. Treatments with DNA nanoparticles (DNPs), which activate STING when cargo DNA is sensed, delayed T1D onset and reduced T1D incidence when administered before T1D onset. DNP treatment elevated indoleamine 2,3 dioxygenase (IDO) activity, which regulates T-cell immunity, in spleen, pancreatic lymph nodes and pancreas of NOD mice. Therapeutic responses to DNPs were partially reversed by inhibiting IDO and DNP treatment synergized with insulin therapy to further delay T1D onset and reduce T1D incidence. Treating pre-diabetic NOD mice with cyclic guanyl-adenyl dinucleotide (cGAMP) to activate STING directly delayed T1D onset and stimulated interferon-αβ (IFN-αβ), while treatment with cyclic diguanyl nucleotide (cdiGMP) did not delay T1D onset or induce IFN-αβ in NOD mice. DNA sequence analyses revealed that NOD mice possess a STING polymorphism that may explain differential responses to cGAMP and cdiGMP. In summary, STING agonists attenuate T1D progression and DNPs enhance therapeutic responses to insulin therapy.

Indexed as

AnimalsCyclic GMPDiabetes Mellitus, Type 1Disease Models, AnimalDNADrug SynergismFemaleHumansIndoleamine-Pyrrole 2,3,-DioxygenaseInsulinMembrane ProteinsMiceMice, Inbred NODNanoparticlesNucleotides, CyclicPolymorphism, Geneticbis(3',5')-cyclic diguanylic acidCyclic GMPcyclic guanosine monophosphate-adenosine monophosphateDNAIndoleamine-Pyrrole 2,3,-DioxygenaseInsulinMembrane ProteinsNucleotides, CyclicSting1 protein, mouseSTING Proteinindoleamine 2,3 dioxygenasestimulator of interferon genestype I diabetes

Identifiers

PMID31557322
PMCPMC6856934
OpenAlexW2976653310

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.