Evidence map›Paper›PMID 26840537›Full record

ArticlePloS one2016

The Role of T Cell Costimulation via DNAM-1 in Kidney Transplantation.

Anna K Kraus, Jin Chen, Ilka Edenhofer, Inga Ravens, Ariana Gaspert, Pietro E Cippà, Steffen Mueller, Rudolf P Wuthrich, Stephan Segerer, Guenter Bernhardt and 1 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

6 citing papers in PubMed, 13 citations in OpenAlex.

  1. Review
  2. Article
  3. TIGIT regulates CD4Frontiers in immunology · 2024
    Article
  4. The Ratio of CD226 and TIGIT Expression in Tfh and PD-1Journal of immunology research · 2022
    Article
  5. CD226: An Emerging Role in Immunologic Diseases.Frontiers in cell and developmental biology · 2020
    Article
  6. 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

11 authors at 4 institutions in 3 countries.

Anna K KrausInstitute of Physiology, University of Zurich, Zurich, Switzerland.
Jin ChenInstitute of Physiology, University of Zurich, Zurich, Switzerland.
Ilka EdenhoferInstitute of Physiology, University of Zurich, Zurich, Switzerland.
Inga RavensInstitute of Immunology, Hannover Medical School, Hannover, Germany.
Ariana GaspertInstitute of Surgical Pathology, University Hospital Zurich, Zurich, Switzerland.
Pietro E CippàDivision of Nephrology, University Hospital Zurich, Zurich, Switzerland.
Steffen MuellerDepartment of Molecular Genetics and Microbiology, Stony Brook University, New York, New York, United States of America.
Rudolf P WuthrichInstitute of Physiology, University of Zurich, Zurich, Switzerland.
Stephan SegererInstitute of Physiology, University of Zurich, Zurich, Switzerland.
Guenter BernhardtInstitute of Immunology, Hannover Medical School, Hannover, Germany.
Thomas FehrInstitute of Physiology, University of Zurich, Zurich, Switzerland.
University Hospital of Zurich · CHUniversity of Zurich · CHMedizinische Hochschule Hannover · DEStony Brook University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

DNAX accessory protein-1 (DNAM-1, CD226) is a co-stimulatory and adhesion molecule expressed mainly by natural killer cells and T cells. DNAM-1 and its two ligands CD112 and CD155 are important in graft-versus-host disease, but their role in solid organ transplantation is largely unknown. We investigated the relevance of this pathway in a mouse kidney transplantation model. CD112 and CD155 are constitutively expressed on renal tubular cells and strongly upregulated in acutely rejected renal allografts. In vitro DNAM-1 blockade during allogeneic priming reduced the allospecific T cell response but not the allospecific cytotoxicity against renal tubular epithelial cells. Accordingly, absence of DNAM-1 in recipient mice or absence of CD112 or CD155 in the kidney allograft did not significantly influence renal function and severity of rejection after transplantation, but led to a higher incidence of infarcts in CD112 and CD155 deficient kidney allografts. Thus, DNAM-1 blockade is not effective in preventing transplant rejection. Despite of being highly expressed, CD112 and CD155 do not appear to play a major immunogenic role in kidney transplantation. Considering the high incidence of renal infarcts in CD112 and CD155 deficient grafts, blocking these molecules might be detrimental.

Indexed as

Kidney TransplantationAllograftsAnimalsAntigens, Differentiation, T-LymphocyteCytotoxicity, ImmunologicEpithelial CellsGene ExpressionGraft RejectionInterleukin-2 Receptor beta SubunitKidney TubulesLigandsLymphocyte ActivationMiceMice, KnockoutModels, AnimalReceptors, VirusAntigens, Differentiation, T-LymphocyteInterleukin-2 Receptor beta SubunitLigandspoliovirus receptorReceptors, VirusT Lineage-Specific Activation Antigen 1

Identifiers

PMID26840537
PMCPMC4739582
OpenAlexW2271212716

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.