Evidence map›Paper›PMID 25807873›Full record

ReviewAmerican journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons2015

Tempering allorecognition to induce transplant tolerance with chemically modified apoptotic donor cells.

D P McCarthy, J Bryant, J P Galvin, S D Miller, X Luo

Abstract readReview
In one paragraph

Review in American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–field-weighted citation impact
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

9 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Receptor tyrosine kinase MerTK suppresses an allogenic type I IFN response to promote transplant tolerance.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2019
    Article
  6. Article
  7. Review
  8. TIGITNature communications · 2018
    Article
  9. 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

5 authors.

D P McCarthyDepartment of Microbiology-Immunology and Interdepartmental Immunobiology Center, Feinberg School of Medicine, Northwestern University, Chicago, IL.
J BryantDepartment of Medicine, Feinberg School of Medicine, Northwestern University, Evanston, IL.
J P GalvinDepartment of Microbiology-Immunology and Interdepartmental Immunobiology Center, Feinberg School of Medicine, Northwestern University, Chicago, IL.
S D MillerDepartment of Microbiology-Immunology and Interdepartmental Immunobiology Center, Feinberg School of Medicine, Northwestern University, Chicago, IL.
X LuoDepartment of Microbiology-Immunology and Interdepartmental Immunobiology Center, Feinberg School of Medicine, Northwestern University, Chicago, IL.

Funding

IMMUNOREGULATION AND PATHOLOGY OF CHRONIC-RELAPSING EAER01NS026543 · NINDS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI MILLER, STEPHEN D · 1988 to 2016
$5.0M
Transplant Surgery Scientist Training ProgramT32DK077662 · NIDDK · NORTHWESTERN UNIVERSITY AT CHICAGO · PI Richard M Green, Daniela P Ladner · 2007 to 2026
$3.8M
NIDDK NIH HHS T32 DK077662NIDDK NIH HHS T32DK077662NINDS NIH HHS R01 NS026543
6 · The paper itself

Abstract

The development of organ transplantation as a therapy for end-stage organ failure is among the most significant achievements of 20th century medicine, but chronic rejection remains a barrier to achieving long-term success. Current therapeutic regimens consist of immunosuppressive drugs that are efficient at delaying rejection but are associated with significant risks such as opportunistic infections, toxicity, and malignancy. Thus, the induction of specific immune tolerance to transplant antigens is the coveted aim of researchers. The use of 1-ethyl-3-(3-dimethylaminopropyl)carbodiimide (ECDI)-treated, autoantigen-coupled syngeneic leukocytes has been developed as a specific immunotherapy in preclinical models of autoimmunity and is currently in a phase II clinical trial for the treatment of multiple sclerosis. In this review, we discuss the use of allogeneic ECDI-treated apoptotic donor leukocytes (allo-ECDI-SP) as a strategy for inducing antigen-specific tolerance in allogeneic transplantation. Allo-ECDI-SP therapy induces long-term systemic immune tolerance to transplant antigens by subverting alloimmune recognition and exploiting apoptotic cell uptake pathways to recapitulate innate mechanisms of peripheral tolerance. Lastly, we discuss potential indications and challenges for transitioning allo-ECDI-SP therapy into clinical practice.

Indexed as

Tissue DonorsAnimalsApoptosisCytokinesEthyldimethylaminopropyl CarbodiimideGraft RejectionHumansImmune ToleranceImmunity, CellularImmunity, InnateImmunotherapyLeukocytesModels, AnimalTransplantation, HomologousTransplantsCytokinesEthyldimethylaminopropyl CarbodiimideBasic (laboratory) research/sciencecell death: apoptosisdendritic cellimmunobiologyislet transplantationT cell biologytolerancetranslational research/science

Identifiers

PMID25807873
PMCPMC4439351

What OpenQuestion holds

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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.