Evidence map›Paper›PMID 17463170›Full record

ArticleBlood2007

Role of CD28 in fatal autoimmune disorder in scurfy mice.

Nagendra Singh, Phillip R Chandler, Yoichi Seki, Babak Baban, Mayuko Takezaki, David J Kahler, David H Munn, Christian P Larsen, Andrew L Mellor, Makio Iwashima

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

21 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Unregulated antigen-presenting cell activation by T cells breaks self tolerance.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  9. Adenosine AFrontiers in immunology · 2017
    Article
  10. Article
  11. B cells are critical for autoimmune pathology in Scurfy mice.Proceedings of the National Academy of Sciences of the United States of America · 2013
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Autoimmune polyglandular syndromes.Nature reviews. Endocrinology · 2010
    Review
  19. Immunologic endocrine disorders.The Journal of allergy and clinical immunology · 2010
    Review
  20. 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

10 authors at 2 institutions in 1 country.

Nagendra SinghImmunotherapy Center, Medical College of Georgia, Augusta, USA.
Phillip R Chandler
Yoichi Seki
Babak Baban
Mayuko Takezaki
David J Kahler
David H Munn
Christian P Larsen
Andrew L Mellor
Makio Iwashima
Augusta University · USEmory University · US

Funding

Spatial control of Ca2+ signals in lymphocytesR01AI055022 · NIAID · MEDICAL COLLEGE OF GEORGIA (MCG) · PI IWASHIMA, MAKIO · 2003 to 2007
$1.4M
Threshold control for T cell antigen receptorK02AI049398 · NIAID · MEDICAL COLLEGE OF GEORGIA (MCG) · PI IWASHIMA, MAKIO · 2001 to 2005
$543k
NIAID NIH HHS AI049398NIAID NIH HHS AI055022NIAID NIH HHS K02 AI049398NIAID NIH HHS R01 AI055022
6 · The paper itself

Abstract

Scurfy mice develop CD4 T-cell-mediated lymphoproliferative disease leading to death within 4 weeks of age. The scurfy mutation causes loss of function of the foxp3 gene (foxp3(sf)), which is essential for development and maintenance of naturally occurring regulatory CD4 T cells (nTregs). In humans, mutations of the foxp3 gene cause immune dysregulation, polyendocrinopathy, enteropathy, and X-linked syndrome (IPEX). In most patients with IPEX and also in scurfy mice, T cells show hyperreactivity and levels of Th1- and Th2-associated cytokines are substantially elevated. We report that removal of CD28 expression rescued scurfy mice from early death. Longer-term surviving CD28-deficient scurfy mice still had lymphoproliferative disorder, but their CD4 T cells showed decreased interferon-gamma and no sign of interleukin-4 or interleukin-10 hyperproduction. Furthermore, injection of CTLA4-Ig to block CD28-B7 interactions substantially improved the survival of scurfy mice by blocking effector T-cell differentiation. These data support the hypothesis that CD28-B7 interactions play a critical role in the etiology of lethal autoimmune disease in scurfy mice by stimulating the differentiation of antigen-activated naive T cells into effector T cells.

Indexed as

Genes, LethalAnimalsAntigens, CDAntigens, DifferentiationAutoimmune DiseasesCD28 AntigensCD4-Positive T-LymphocytesCell ProliferationCTLA-4 AntigenCytokinesFemaleForkhead Transcription FactorsHumansImmunoglobulin GInterferon-gammaInterleukin-10Antigens, CDAntigens, DifferentiationCD28 AntigensCTLA-4 AntigenCTLA4 protein, humanCtla4 protein, mouseCytokinesForkhead Transcription FactorsFoxp3 protein, mouseImmunoglobulin GInterferon-gammaInterleukin-10Interleukin-4

Identifiers

PMID17463170
PMCPMC1939901
OpenAlexW1975322648

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.