Evidence map›Paper›PMID 23593209›Full record

ArticlePloS one2013

CD160Ig fusion protein targets a novel costimulatory pathway and prolongs allograft survival.

Francesca D'Addio, Takuya Ueno, Michael Clarkson, Baogong Zhu, Andrea Vergani, Gordon J Freeman, Mohamed H Sayegh, Mohammed Javeed I Ansari, Paolo Fiorina, Antje Habicht

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

16 citing papers in PubMed, 27 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. miR-21 antagonism reprograms macrophage metabolism and abrogates chronic allograft vasculopathy.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2021
    Article
  6. Article
  7. CD160 Stimulates CD8ImmunoHorizons · 2018
    Article
  8. Article
  9. Associations betweenOncotarget · 2017
    Article
  10. Article
  11. T Cells Going Innate.Trends in immunology · 2016
    Review
  12. Article
  13. Article
  14. CD160 is essential for NK-mediated IFN-γ production.The Journal of experimental medicine · 2015
    Article
  15. Review
  16. 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

10 authors at 3 institutions in 4 countries.

Francesca D'AddioTransplantation Research Center, Renal Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, United States of America.
Takuya Ueno
Michael Clarkson
Baogong Zhu
Andrea Vergani
Gordon J Freeman
Mohamed H Sayegh
Mohammed Javeed I Ansari
Paolo Fiorina
Antje Habicht
Brigham and Women's Hospital · USHarvard University · USDana-Farber Cancer Institute · US

Funding

Transgenic/KnockoutP01AI056299 · NIAID · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI BLAZAR, BRUCE R · 2003 to 2023
$42.5M
Role of Novel Th17 cells in allograft rejection and toleranceK08AI080836 · NIAID · NORTHWESTERN UNIVERSITY AT CHICAGO · PI ANSARI, MOHAMMED JAVEED · 2009 to 2013
$631k
NIAID NIH HHS AI1051559NIAID NIH HHS AI56299NIAID NIH HHS K08 AI080836NIAID NIH HHS K08 AI080836-01NIAID NIH HHS P01 AI056299
6 · The paper itself

Abstract

CD160 is a cell surface molecule expressed by most NK cells and approximately 50% of CD8(+) cytotoxic T lymphocytes. Engagement of CD160 by MHC class-I directly triggers a costimulatory signal to TCR-induced proliferation, cytokine production and cytotoxic effector functions. The role of CD160 in alloimmunity is unknown. Using a newly generated CD160 fusion protein (CD160Ig) we examined the role of the novel costimulatory molecule CD160 in mediating CD4(+) or CD8(+) T cell driven allograft rejection. CD160Ig inhibits alloreactive CD8(+) T cell proliferation and IFN-γ production in vitro, in particular in the absence of CD28 costimulation. Consequently CD160Ig prolongs fully mismatched cardiac allograft survival in CD4(-/-), CD28(-/-) knockout and CTLA4Ig treated WT recipients, but not in WT or CD8(-/-) knockout recipients. The prolonged cardiac allograft survival is associated with reduced alloreactive CD8(+) T cell proliferation, effector/memory responses and alloreactive IFN-γ production. Thus, CD160 signaling is particularly important in CD28-independent effector/memory CD8(+) alloreactive T cell activation in vivo and therefore may serve as a novel target for prevention of allograft rejection.

Indexed as

AnimalsAntigen-Presenting CellsAntigens, CDCD28 AntigensCD4 AntigensCytokinesCytotoxicity, ImmunologicGene ExpressionGPI-Linked ProteinsGraft SurvivalHeart TransplantationHistocompatibility Antigens Class IImmunoglobulin GImmunologic MemoryInterferon-gammaKiller Cells, NaturalAntigens, CDCD160 protein, humanCD28 AntigensCD4 AntigensCytokinesGPI-Linked ProteinsHistocompatibility Antigens Class IImmunoglobulin GInterferon-gammaReceptors, ImmunologicRecombinant Fusion Proteins

Identifiers

PMID23593209
PMCPMC3617215
OpenAlexW2140041178

What OpenQuestion holds

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Registered trials

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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.