Evidence map›Paper›PMID 23042535›Full record

ArticleCellular & molecular immunology2012

Treg cells in pancreatic lymph nodes: the possible role in diabetogenesis and β cell regeneration in a T1D model.

Benjamin K Nti, Janet L Markman, Suzanne Bertera, Alexis J Styche, Robert J Lakomy, Vladimir M Subbotin, Massimo Trucco, Tatiana D Zorina

Open access · bronzeAbstract read
In one paragraph

Article in Cellular & molecular immunology, 2012. 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
2.4field-weighted citation impact, top 12% 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, 32 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Nanotargeted Delivery of Immune Therapeutics in Type 1 Diabetes.Advanced materials (Deerfield Beach, Fla.) · 2023
    Article
  5. Review
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  12. Review
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  14. CXCL12 protects pancreatic β-cells from oxidative stress by a Nrf2-induced increase in catalase expression and activity.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2016
    Article
  15. Article
  16. Review
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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

8 authors at 5 institutions in 1 country.

Benjamin K NtiIndiana University School of Medicine, Indianapolis, IN, USA.
Janet L Markman
Suzanne Bertera
Alexis J Styche
Robert J Lakomy
Vladimir M Subbotin
Massimo Trucco
Tatiana D Zorina
Children's Hospital of Pittsburgh · USUniversity of Pittsburgh · USCedars-Sinai Medical Center · USIndiana University School of MedicineThomas Jefferson University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Previously, we established a model in which physiologically adequate function of the autologous β cells was recovered in non-obese diabetic (NOD) mice after the onset of hyperglycemia by rendering them hemopoietic chimera. These mice were termed antea-diabetic. In the current study, we addressed the role of T regulatory (Treg) cells in the mechanisms mediating the restoration of euglycemia in the antea-diabetic NOD model. The data generated in this study demonstrated that the numbers of Treg cells were decreased in unmanipulated NOD mice, with the most profound deficiency detected in the pancreatic lymph nodes (PLNs). The impaired retention of the Treg cells in the PLNs correlated with the locally compromised profile of the chemokines involved in their trafficking, with the most prominent decrease observed in SDF-1. The amelioration of autoimmunity and restoration of euglycemia observed in the antea-diabetic mice was associated with restoration of the Treg cell population in the PLNs. These data indicate that the function of the SDF-1/CXCR4 axis and the retention of Treg cells in the PLNs have a potential role in diabetogenesis and in the amelioration of autoimmunity and β cell regeneration in the antea-diabetic model. We have demonstrated in the antea-diabetic mouse model that lifelong recovery of the β cells has a strong correlation with normalization of the Treg cell population in the PLNs. This finding offers new opportunities for testing the immunomodulatory regimens that promote accumulation of Treg cells in the PLNs as a therapeutic approach for type 1 diabetes (T1D).

Indexed as

AnimalsCell CountCell MovementChemokinesDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 1Disease Models, AnimalForkhead Transcription FactorsHistocompatibility Antigens Class IImmune ToleranceInsulin-Secreting CellsLymph NodesMiceMice, Inbred NODRegenerationT-Lymphocytes, RegulatoryChemokinesForkhead Transcription FactorsFoxp3 protein, mouseHistocompatibility Antigens Class I

Identifiers

PMID23042535
PMCPMC4002217
OpenAlexW1998035513

What OpenQuestion holds

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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.