Evidence map›Paper›PMID 18250428›Full record

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

Anti-MHC class I antibody activation of proliferation and survival signaling in murine cardiac allografts.

Peter T Jindra, Aileen Hsueh, Longshen Hong, David Gjertson, Xiu-Da Shen, Feng Gao, Julie Dang, Paul S Mischel, William M Baldwin, Michael C Fishbein and 2 more

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 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

61 citing papers in PubMed, 96 citations in OpenAlex.

  1. Review
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  8. The natural killer cell activating receptor, NKG2D, is critical to antibody-dependent chronic rejection in heart transplantation.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2021
    Article
  9. Sensitization in transplantation: Assessment of risk (STAR) 2019 Working Group Meeting Report.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2020
    Review
  10. Antibody-induced vascular inflammation skews infiltrating macrophages to a novel remodeling phenotype in a model of transplant rejection.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2020
    Article
  11. Review
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  14. Outside-in HLA class I signaling regulates ICAM-1 clustering and endothelial cell-monocyte interactions via mTOR in transplant antibody-mediated rejection.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2018
    Article
  15. Review
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  20. Review

1 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

12 authors at 2 institutions in 1 country.

Peter T JindraUCLA Immunogenetics Center and Department of Pathology and Laboratory Medicine, David Geffen School of Medicine, University of California-Los Angeles, 1000 Veteran Avenue, Los Angeles, CA 90095, USA.
Aileen Hsueh
Longshen Hong
David Gjertson
Xiu-Da Shen
Feng Gao
Julie Dang
Paul S Mischel
William M Baldwin
Michael C Fishbein
Jerzy W Kupiec-Weglinski
Elaine F Reed
University of California, Los Angeles · USJohns Hopkins University · US

Funding

Anti-MHC Effects on EndotheliumR01AI042819 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI REED, ELAINE F · 1999 to 2014
$4.0M
INFECTIOUS TOLERANCE IN TRANSPLANT RECIPIENTSR01AI042223 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI KUPIEC-WEGLINSKI, JERZY W · 1998 to 2008
$2.4M
NOVEL THERAPIES FOR GRAFT REJECTION IN SENSITIZED HOSTSR01AI023847 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI KUPIEC-WEGLINSKI, JERZY W. · 1988 to 2006
$1.8M
NIAID NIH HHS R01 AI023847NIAID NIH HHS R01 AI042223NIAID NIH HHS R01 AI042819NIAID NIH HHS R01 AI 23847NIAID NIH HHS R01 AI 42223NIAID NIH HHS R01 AI 42819
6 · The paper itself

Abstract

Anti-MHC class I alloantibodies have been implicated in the process of acute and chronic rejection because these Abs can bind to endothelial cells and transduce signals leading to the activation of cell survival and proliferation pathways. To characterize the role of the MHC class I-signaling pathway in the pathogenesis of Ab-mediated rejection, we developed a mouse vascularized heterotopic cardiac allograft model in which B6.RAG1 KO hosts (H-2K(b)/D(b)) received a fully MHC-incompatible BALB/c (H-2K(d)/D(d)) heart transplant and were passively transfused with anti-donor MHC class I Ab. We demonstrate that cardiac allografts of mice treated with anti-MHC class I Abs show characteristic features of Ab-mediated rejection including microvascular changes accompanied by C4d deposition. Phosphoproteomic analysis of signaling molecules involved in the MHC class I cell proliferation and survival pathways were elevated in anti-class I-treated mice compared with the isotype control-treated group. Pairwise correlations, hierarchical clustering, and multidimensional scaling algorithms were used to dissect the class I-signaling pathway in vivo. Treatment with anti-H-2K(d) Ab was highly correlated with the activation of Akt and p70S6Kinase (S6K). When measuring distance as a marker of interrelatedness, multidimensional scaling analysis revealed a close association between members of the mammalian target of rapamycin pathway including mammalian target of rapamycin, S6K, and S6 ribosomal protein. These results provide the first analysis of the interrelationships between these signaling molecules in vivo that reflects our knowledge of the signaling pathway derived from in vitro experiments.

Indexed as

Cell ProliferationAnimalsAntibodies, MonoclonalCell SurvivalExtracellular Signal-Regulated MAP KinasesGraft RejectionH-2 AntigensHeart TransplantationHistocompatibility Antigen H-2DImmunization, PassiveIsoantibodiesMaleMAP Kinase Signaling SystemMiceMice, Inbred BALB CMice, Inbred C57BLAntibodies, MonoclonalExtracellular Signal-Regulated MAP KinasesH-2 AntigensH-2Kb protein, mouseH-2K(K) antigenHistocompatibility Antigen H-2DIsoantibodies

Identifiers

PMID18250428
PMCPMC3883756
OpenAlexW1580674042

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.