Evidence map›Paper›PMID 18079964›Full record

ArticleThe Journal of clinical investigation2008

Immunostimulatory Tim-1-specific antibody deprograms Tregs and prevents transplant tolerance in mice.

Nicolas Degauque, Christophe Mariat, James Kenny, Dong Zhang, Wenda Gao, Minh Diem Vu, Sophoclis Alexopoulos, Mohammed Oukka, Dale T Umetsu, Rosemarie H DeKruyff and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed
6.5field-weighted citation impact, top 3% 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

71 citing papers in PubMed, 120 citations in OpenAlex.

  1. Synergistic venetoclax and anti-CD3 therapy for control of alloreactive response in hematopoietic stem cell transplantation.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2026
    Article
  2. Review
  3. Review
  4. Review
  5. Review
  6. Role of TIM-1 in the development and treatment of tumours.Frontiers in cell and developmental biology · 2024
    Review
  7. Review
  8. Review
  9. Review
  10. Review
  11. Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. TIM-3 and TIM-1 Could Regulate DecidualJournal of immunology research · 2019
    Article
  17. Article
  18. Virological and Immunological Outcomes of Coinfections.Clinical microbiology reviews · 2018
    Review
  19. Article
  20. Review

11 more citing papers are in PubMed but not listed here.

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

13 authors at 2 institutions in 1 country.

Nicolas DegauqueDivision of Transplant Immunology and Transplant Research Center, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02115, USA.
Christophe Mariat
James Kenny
Dong Zhang
Wenda Gao
Minh Diem Vu
Sophoclis Alexopoulos
Mohammed Oukka
Dale T Umetsu
Rosemarie H DeKruyff
Vijay Kuchroo
Xin Xiao Zheng
Terry B Strom
Harvard University Press · USHarvard University · US

Funding

Trafficking and the role of myelin specific Regulatory T cells in EAER01AI073542 · NIAID · SEATTLE CHILDREN'S HOSPITAL · PI OUKKA, MOHAMED · 2007 to 2011
$2.2M
NIAID NIH HHS R01 AI073542
6 · The paper itself

Abstract

T cell Ig mucin (Tim) molecules modulate CD4(+) T cell responses. In keeping with the view that Tim-1 generates a stimulatory signal for CD4(+) T cell activation, we hypothesized that an agonist Tim-1-specific mAb would intensify the CD4(+) T cell-dependant allograft response. Unexpectedly, we determined that a particular Tim-1-specific mAb exerted reciprocal effects upon the commitment of alloactivated T cells to regulatory and effector phenotypes. Commitment to the Th1 and Th17 phenotypes was fostered, whereas commitment to the Treg phenotype was hindered. Moreover, ligation of Tim-1 in vitro effectively deprogrammed Tregs and thus produced Tregs unable to control T cell responses. Overall, the effects of the agonist Tim-1-specific mAb on the allograft response stemmed from enhanced expansion and survival of T effector cells; a capacity to deprogram natural Tregs; and inhibition of the conversion of naive CD4(+) T cells into Tregs. The reciprocal effects of agonist Tim-1-specific mAbs upon effector T cells and Tregs serve to prevent allogeneic transplant tolerance.

Indexed as

AnimalsAntibodies, MonoclonalGraft SurvivalHepatitis A Virus Cellular Receptor 1Interleukin-17Islets of Langerhans TransplantationLymphocyte ActivationMembrane ProteinsMiceT-Lymphocytes, Helper-InducerT-Lymphocytes, RegulatoryTransplantation ToleranceAntibodies, MonoclonalHavcr1 protein, mouseHepatitis A Virus Cellular Receptor 1Interleukin-17Membrane Proteins

Identifiers

PMID18079964
PMCPMC2129234
OpenAlexW2135004938

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.