Evidence map›Paper›PMID 21745722›Full record

ArticleJournal of autoimmunity2011

IL-7 uniquely maintains FoxP3(+) adaptive Treg cells that reverse diabetes in NOD mice via integrin-β7-dependent localization.

Cheng-Rui Li, Mia F Deiro, Elana Godebu, Linda M Bradley

Open access · greenAbstract read
In one paragraph

Article in Journal of autoimmunity, 2011. 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
1.5field-weighted citation impact, top 18% 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, 27 citations in OpenAlex.

  1. Article
  2. Review
  3. Role of Interleukins in Type 1 and Type 2 Diabetes.Diagnostics (Basel, Switzerland) · 2025
    Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Liver immunology.Comprehensive Physiology · 2013
    Review
  15. Article
  16. Autoimmunity in 2011.Clinical reviews in allergy & immunology · 2012
    Review
  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

4 authors at 2 institutions in 1 country.

Cheng-Rui LiInfectious and Inflammatory Disease Center, Sanford-Burnham Medical Research Institute, La Jolla, CA 92037, USA.
Mia F Deiro
Elana Godebu
Linda M Bradley
Sanford Burnham Prebys Medical Discovery Institute · USUniversity of California, San Diego · US

Funding

CD4 T Cell Subsets in Type 1 DiabetesR21AI081238 · NIAID · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI BRADLEY, LINDA MAC PHERSON · 2009 to 2010
$525k
NIAID NIH HHS AI081238NIAID NIH HHS R21 AI081238
6 · The paper itself

Abstract

Type 1 diabetes (T1D) develops as a consequence of a progressive autoimmune response that destroys insulin-producing β-cells in pancreatic islets. Because of their role(s) in controlling immune responses, considerable effort has been directed toward resolving whether regulatory T cells (Tregs) offer a clinical treatment to restore tolerance in T1D. We previously reported that in vitro-induced adaptive Treg cells (aTregs) can reverse T1D and persist as protective memory cells in the NOD mouse model. In the current study, we investigated mechanisms that regulate aTregs. We found that these FoxP3(+) aTregs expressed high levels of the IL-7 receptor, IL-7Rα, without the high affinity receptor for IL-2, CD25, which is found on natural Treg cells (nTregs). IL-7Rα expression was mirrored by the dependency of aTregs on IL-7 for persistence. IL-10 and TGF-β, effector cytokines of aTregs, were not essential for their maintenance at the level of systemic antibody blocking. Nevertheless, IL-10 modulated cytokine production by aTregs and TGF-β was critical for protection. aTregs were found to infiltrate islets and the expression of integrin-β7 was required for their localization in the pancreas. Furthermore, blocking aTreg entry into the pancreas prevented their control of diabetogenic effector T cells, implying the need for local control of the autoimmune response. The distinct homeostatic regulation of aTregs independently of a response to IL-2, which is defective in T1D patients, suggests that these cells represent a translatable candidate to control the autoimmune response.

Indexed as

Adaptive ImmunityT-Lymphocytes, RegulatoryAdoptive TransferAnimalsAutoimmunityCell DifferentiationCell MovementDiabetes Mellitus, Type 1FemaleHumansIntegrin beta ChainsInterleukin-10Interleukin-2Interleukin-2 Receptor alpha SubunitInterleukin-7MiceIl2ra protein, mouseintegrin beta7Integrin beta ChainsInterleukin-10Interleukin-2Interleukin-2 Receptor alpha SubunitInterleukin-7interleukin-7 receptor, alpha chainReceptors, Interleukin-7Transforming Growth Factor beta

Identifiers

PMID21745722
PMCPMC3431214
OpenAlexW2142566291

What OpenQuestion holds

Textmetadata
LicenceTDM
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.