Evidence map›Paper›PMID 18606676›Full record

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

Critical role of effector macrophages in mediating CD4-dependent alloimmune injury of transplanted liver parenchymal cells.

Phillip H Horne, Jason M Zimmerer, Mason G Fisher, Keri E Lunsford, Gyongyi Nadasdy, Tibor Nadasdy, Nico van Rooijen, Ginny L Bumgardner

Open access · hybridAbstract 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 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

15 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
  2. Macrophage depletion of CMV latently infected donor hearts ameliorates recipient accelerated chronic rejection.Transplant infectious disease : an official journal of the Transplantation Society · 2021
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Immunological aspects of liver cell transplantation.World journal of transplantation · 2016
    Review
  9. Critical role of NKT cells in posttransplant alloantibody production.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2014
    Article
  10. Effector mechanisms of rejection.Cold Spring Harbor perspectives in medicine · 2013
    Review
  11. Article
  12. Article
  13. Article
  14. Characterization of immune responses to cardiac self-antigens myosin and vimentin in human cardiac allograft recipients with antibody-mediated rejection and cardiac allograft vasculopathy.The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation · 2010
    Article
  15. 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

8 authors at 3 institutions in 2 countries.

Phillip H HorneDepartment of Surgery, Comprehensive Transplant Center, Ohio State University Medical Center, Columbus, OH 43210, USA.
Jason M Zimmerer
Mason G Fisher
Keri E Lunsford
Gyongyi Nadasdy
Tibor Nadasdy
Nico van Rooijen
Ginny L Bumgardner
Integrated Oncology (United States) · USThe Ohio State University Wexner Medical Center · USVrije Universiteit Amsterdam · NL

Funding

Pre-Conditioning Pancreatic Islets for TransplantationR21DK072262 · NIDDK · OHIO STATE UNIVERSITY · PI BUMGARDNER, GINNY L · 2005 to 2006
$406k
NIDDK NIH HHS DK072262NIDDK NIH HHS R21 DK072262
6 · The paper itself

Abstract

Despite the recognition that humoral rejection is an important cause of allograft injury, the mechanism of Ab-mediated injury to allograft parenchyma is not well understood. We used a well-characterized murine hepatocellular allograft model to determine the mechanism of Ab-mediated destruction of transplanted liver parenchymal cells. In this model, allogeneic hepatocytes are transplanted into CD8-deficient hosts to focus on CD4-dependent, alloantibody-mediated rejection. Host serum alloantibody levels correlated with in vivo allospecific cytotoxic activity in CD8 knockout hepatocyte rejector mice. Host macrophage depletion, but not CD4(+) T cell, NK cell, neutrophil, or complement depletion, inhibited in vivo allocytotoxicity. Recipient macrophage deficiency delayed CD4-dependent hepatocyte rejection and inhibited in vivo allocytotoxicity without influencing alloantibody production. Furthermore, hepatocyte coincubation with alloantibody and macrophages resulted in Ab-dependent hepatocellular cytotoxicity in vitro. These studies are consistent with a paradigm of acute humoral rejection in which CD4(+) T cell-dependent alloantibody production results in the targeting of transplanted allogeneic parenchymal cells for macrophage-mediated cytotoxic immune damage. Consequently, strategies to eliminate recipient macrophages during CD4-dependent rejection pathway may prolong allograft survival.

Indexed as

AnimalsCD4-Positive T-LymphocytesGraft RejectionGraft SurvivalHepatocytesIsoantibodiesLiver TransplantationMacrophagesMiceMice, KnockoutMice, Mutant StrainsTransplantation, HomologousIsoantibodies

Identifiers

PMID18606676
PMCPMC3022512
OpenAlexW1688209769

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.