Evidence map›Paper›PMID 19036642›Full record

ArticleClinical immunology (Orlando, Fla.)2009

APC dysfunction is correlated with defective suppression of T cell proliferation in human type 1 diabetes.

Yulan Jin, Xueqin Chen, Robert Podolsky, Diane Hopkins, Levi H C Makala, Andy Muir, Jin-Xiong She

Open access · greenAbstract read
In one paragraph

Article in Clinical immunology (Orlando, Fla.), 2009. 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
0.7field-weighted citation impact, top 31% 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. Review
  2. Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Translating Treg Therapy in Humanized Mice.Frontiers in immunology · 2015
    Review
  10. Advances in the cellular immunological pathogenesis of type 1 diabetes.Journal of cellular and molecular medicine · 2014
    Review
  11. Impairment of regulatory T-cell function in autoimmune thyroid disease.Thyroid : official journal of the American Thyroid Association · 2013
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. 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

7 authors at 1 institution in 1 country.

Yulan JinCenter for Biotechnology and Genomic Medicine, Medical College of Georgia, Augusta, GA 30912, USA.
Xueqin Chen
Robert Podolsky
Diane Hopkins
Levi H C Makala
Andy Muir
Jin-Xiong She
Augusta University · US

Funding

The TEDDY Study: Georgia/Florida Clinical CenterUC4DK063865 · NIDDK · AUGUSTA UNIVERSITY · PI SHE, JIN-XIONG · 2013 to 2013
$5.3M
Studies of the Immunopathogenesis of Type 1 DiabetesR01HD037800 · NICHD · UNIVERSITY OF FLORIDA · PI SHE, JIN-XIONG · 1999 to 2006
$4.6M
NIDDK BIOTECHNOLOGY CENTER AT THE UNIVERSITY OF FLORIDAU24DK058778 · NIDDK · UNIVERSITY OF FLORIDA · PI SHE, JIN-XIONG · 2000 to 2002
$1.7M
Proteomic changes/progression of human type 1 diabetesR33HD050196 · NICHD · AUGUSTA UNIVERSITY · PI SHE, JIN-XIONG · 2006 to 2008
$1.5M
Development of microarray-based biomarkers for type 1 diR33DK069878 · NIDDK · AUGUSTA UNIVERSITY · PI SHE, JIN-XIONG · 2006 to 2008
$1.1M
Development of microarray-based biomarkers for type 1 diR21DK069878 · NIDDK · MEDICAL COLLEGE OF GEORGIA (MCG) · PI SHE, JIN-XIONG · 2004 to 2005
$733k
Proteomic changes/progression of human type 1 diabetesR21HD050196 · NICHD · MEDICAL COLLEGE OF GEORGIA (MCG) · PI SHE, JIN-XIONG · 2004 to 2005
$715k
NICHD NIH HHS 2R01HD37800NICHD NIH HHS 4R33HD050196NICHD NIH HHS R01 HD037800NICHD NIH HHS R21 HD050196NICHD NIH HHS R33 HD050196NIDDK NIH HHS 4R33DK069878NIDDK NIH HHS 5U24DK58778NIDDK NIH HHS R21 DK069878NIDDK NIH HHS R33 DK069878NIDDK NIH HHS U24 DK058778NIDDK NIH HHS UC4 DK063865
6 · The paper itself

Abstract

It is widely believed that CD4(+)CD25(+) regulatory T cells (Treg) are defective in type 1 diabetes (T1D) and other autoimmune diseases. However, this conclusion is based on the suboptimal in vitro suppression results from very small numbers of subjects. Furthermore, the cells responsible for the suboptimal suppression have not been defined. Therefore, we carried out extensive in vitro suppression assays using both autologous and heterologous donors of Tregs, effector T cells and antigen-presenting cells (APC) from both T1D patients and normal controls. Our in vitro suppression data indicated that a significantly higher proportion (40.0%) of T1D patients have "very low suppression" activity (defined as<25%) by autologous Treg compared to controls (6.3%) (p=0.002). Meta-analysis of the published results confirmed this observation with 45.7% low suppressors in T1D and 7.8% in controls (p=0.00002). Interestingly, suppression assays using heterologous Tregs, effector T cells and APC suggest that the source of APC is correlated with the suppression activity. The frequencies of CD4(+)CD25(+) and CD4(+)CD25(hi) T cells were found to increase with age in normal controls but not in T1D patients, resulting in significantly higher frequencies of CD4(+)CD25(+) (p=0.001) and CD4(+)CD25(hi) (p=0.009) T cells in young T1D subjects than age-matched controls but slightly lower CD4(+)CD25(+) (p=0.003) and CD4(+)CD25(hi) (p=0.08) T cells in old T1D subjects than age-matched controls.

Indexed as

Lymphocyte ActivationAdolescentAdultAntigen-Presenting CellsCD4-Positive T-LymphocytesCell ProliferationCells, CulturedChildChild, PreschoolDiabetes Mellitus, Type 1FemaleHumansInfantInterleukin-2 Receptor alpha SubunitMaleMiddle AgedInterleukin-2 Receptor alpha Subunit

Identifiers

PMID19036642
PMCPMC2671725
OpenAlexW2021414400

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.