Evidence map›Paper›PMID 18606644›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2008

Induction of tolerance to cardiac allografts using donor splenocytes engineered to display on their surface an exogenous fas ligand protein.

Esma S Yolcu, Xiao Gu, Chantale Lacelle, Hong Zhao, Laura Bandura-Morgan, Nadir Askenasy, Haval Shirwan

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
0.9field-weighted citation impact, top 24% 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

20 citing papers in PubMed, 33 citations in OpenAlex.

  1. Decoding TNF receptor superfamily control of CD4Cell communication and signaling : CCS · 2026
    Review
  2. Article
  3. Review
  4. Article
  5. Engineering pancreatic islets with a novel form of thrombomodulin protein to overcome early graft loss triggered by instant blood-mediated inflammatory reaction.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2023
    Article
  6. Article
  7. Review
  8. Article
  9. Pancreatic islets engineered with a FasL protein induce systemic tolerance at the induction phase that evolves into long-term graft-localized immune privilege.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2020
    Article
  10. Article
  11. Review
  12. Novel technologies to engineer graft for tolerance induction.Current opinion in organ transplantation · 2016
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Fas mediates cardiac allograft acceptance in mice with impaired T-cell-intrinsic NF-kappaB signaling.Transplant international : official journal of the European Society for Organ Transplantation · 2009
    Article
  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

7 authors at 3 institutions in 3 countries.

Esma S YolcuDepartment of Microbiology and Immunology, Institute for Cellular Therapeutics, University of Louisville, Louisville, KY 40202, USA. e0yolc01@gwise.louisville.edu
Xiao Gu
Chantale Lacelle
Hong Zhao
Laura Bandura-Morgan
Nadir Askenasy
Haval Shirwan
Cellular Therapeutics (United Kingdom) · GBUniversity of Louisville · USSchneider Children's Medical Center · IL

Funding

Allograft Tolerance with Fas/FasL-Mediated ApoptosisR01AI047864 · NIAID · UNIVERSITY OF LOUISVILLE · PI SHIRWAN, HAVAL · 2002 to 2005
$1.1M
APOPTOSIS:A MEANS OF IMMUNE REGULATION TO TREAT DIABETESR21DK061333 · NIDDK · UNIVERSITY OF LOUISVILLE · PI SHIRWAN, HAVAL · 2001 to 2003
$648k
A Novel Approach to Prevent and Treat Type 1 DiabetesR21AI057903 · NIAID · UNIVERSITY OF LOUISVILLE · PI SHIRWAN, HAVAL · 2004 to 2005
$588k
Engineering Bone Marrow Cells for ImmunotherapyR21HL080108 · NHLBI · UNIVERSITY OF LOUISVILLE · PI YOLCU, ESMA S · 2005 to 2006
$399k
NHLBI NIH HHS R21 HL080108NIAID NIH HHS R01 AI047864NIAID NIH HHS R01 AI47864NIAID NIH HHS R21 AI057903NIDDK NIH HHS R21 DK061333NIDDK NIH HHS R21 DK61333
6 · The paper itself

Abstract

The critical role played by Fas ligand (FasL) in immune homeostasis renders this molecule an attractive target for immunomodulation to achieve tolerance to auto- and transplantation Ags. Immunomodulation with genetically modified cells expressing FasL was shown to induce tolerance to alloantigens. However, genetic modification of primary cells in a rapid, efficient, and clinically applicable manner proved challenging. Therefore, we tested the efficacy of donor splenocytes rapidly and efficiently engineered to display on their surface a chimeric form of FasL protein (SA-FasL) for tolerance induction to cardiac allografts. The i.p. injection of ACI rats with Wistar-Furth rat splenocytes displaying SA-FasL on their surface resulted in tolerance to donor, but not F344 third-party cardiac allografts. Tolerance was associated with apoptosis of donor reactive T effector cells and induction/expansion of CD4(+)CD25(+)FoxP3(+) T regulatory (Treg) cells. Treg cells played a critical role in the observed tolerance as adoptive transfer of sorted Treg cells from long-term graft recipients into naive unmanipulated ACI rats resulted in indefinite survival of secondary Wistar-Furth grafts. Immunomodulation with allogeneic cells rapidly and efficiently engineered to display on their surface SA-FasL protein provides an effective and clinically applicable means of cell-based therapy with potential application to regenerative medicine, transplantation, and autoimmunity.

Indexed as

Transplantation ToleranceAdoptive TransferAnimalsCell ProliferationFas Ligand ProteinGraft RejectionGraft SurvivalHeart TransplantationInterferon-gammaMaleRatsRats, Inbred ACIRats, Inbred F344Rats, Inbred WFRecombinant Fusion ProteinsSpleenFas Ligand ProteinInterferon-gammaRecombinant Fusion Proteins

Identifiers

PMID18606644
PMCPMC2593473
OpenAlexW2129966490

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.