Evidence map›Paper›PMID 15173889›Full record

ArticleThe Journal of clinical investigation2004

CD28 ligation induces transplantation tolerance by IFN-gamma-dependent depletion of T cells that recognize alloantigens.

Xue-Zhong Yu, Michael H Albert, Paul J Martin, Claudio Anasetti

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

25 citing papers in PubMed, 67 citations in OpenAlex.

  1. Article
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  8. Review
  9. Immunotherapies: the blockade of inhibitory signals.International journal of biological sciences · 2012
    Review
  10. Article
  11. Selective CD28 blockade attenuates acute and chronic rejection of murine cardiac allografts in a CTLA-4-dependent manner.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2011
    Article
  12. Article
  13. Review
  14. IFN-gamma triggered STAT1-PKB/AKT signalling pathway influences the function of alloantigen reactive regulatory T cells.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2010
    Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. CD28 controls differentiation of regulatory T cells from naive CD4 T cells.Journal of immunology (Baltimore, Md. : 1950) · 2008
    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

4 authors at 2 institutions in 1 country.

Xue-Zhong YuHuman Immunogenetics Program, Clinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA. xyu@fhcrc.org
Michael H Albert
Paul J Martin
Claudio Anasetti
Fred Hutch Cancer Center · USUniversity of Washington · US

Funding

VIRUS-MEDIATED MYELOSUPPRESSIONP01CA018029 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI Geoffrey Roger HILL · 1985 to 2026
$128.4M
Antigen Specific T Cell Tolerance by Anti CD3 AntibodiesR01AI051693 · NIAID · H. LEE MOFFITT CANCER CTR &RES INST · PI ANASETTI, CLAUDIO · 2002 to 2006
$1.8M
ALLO SPECIFIC TOLERANCE BY TARGETING CD28K01CA084132 · NCI · H. LEE MOFFITT CANCER CTR &RES INST · PI YU, XUE-ZHONG · 2000 to 2004
$589k
NCI NIH HHS CA-18029NCI NIH HHS CA-84132NCI NIH HHS K01 CA084132NCI NIH HHS P01 CA018029NIAID NIH HHS AI-51396NIAID NIH HHS R01 AI051693
6 · The paper itself

Abstract

Administration of an agonistic anti-CD28 mAb paradoxically inhibits donor T cell expansion and prevents graft-versus-host disease (GVHD) in mice. Here we examined the mechanism of anti-CD28-mediated immunosuppression and found that anti-CD28 mAb activated, rather than blocked, CD28-mediated signaling in vivo. Anti-CD28 treatment prevented GVHD by selectively depleting alloantigen-activated donor T cells through apoptosis but spared the T cells that did not recognize recipient alloantigens. Overexpression of Bcl-x(L) did not protect T cells from depletion and did not affect GVHD prevention after anti-CD28 treatment. Depletion of activated T cells mediated through CD28 did not depend on the expression of death receptors Fas and TNF receptors type I and II, but both the depletion of activated T cells and the suppressive effect of anti-CD28 mAb on GVHD lethality required donor-derived IFN-gamma production. This study demonstrates that agonistic Ab's specific for the CD28 costimulatory molecule may be used as novel therapeutic agents to abrogate pathogenic T cell responses by selective depletion of activated T cells.

Indexed as

AnimalsAntibodiesB7-1 Antigenbcl-X ProteinCD28 AntigensCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesGraft vs Host DiseaseImmune ToleranceInterferon-gammaIsoantigensMiceProto-Oncogene Proteins c-bcl-2T-LymphocytesAntibodiesB7-1 AntigenBcl2l1 protein, mousebcl-X ProteinCD28 AntigensInterferon-gammaIsoantigensProto-Oncogene Proteins c-bcl-2

Identifiers

PMID15173889
PMCPMC419490
OpenAlexW2072538780

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.