Evidence map›Paper›PMID 26322044›Full record

ReviewFrontiers in immunology2015

Co-Stimulatory Blockade of the CD28/CD80-86/CTLA-4 Balance in Transplantation: Impact on Memory T Cells?

Simon Ville, Nicolas Poirier, Gilles Blancho, Bernard Vanhove

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

31 citing papers in PubMed, 56 citations in OpenAlex.

  1. Trial
  2. Review
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  4. Article
  5. Review
  6. Palmitoylation modulates antitumor immunity.Molecular biology reports · 2025
    Review
  7. Article
  8. Article
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  10. Review
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  13. The single-cell transcriptome of mTECs and CD4Frontiers in immunology · 2024
    Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Review
  19. (Im)maturity in Tumor Ecosystem.Frontiers in oncology · 2021
    Review
  20. 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

4 authors at 2 institutions in 1 country.

Simon VilleUnité Mixte de Recherche, UMR_S 1064, Institut National de la Santé et de la Recherche Médicale , Nantes , France ; Institut de Transplantation Urologie Néphrologie (ITUN), Université de Nantes , Nantes , France.
Nicolas PoirierUnité Mixte de Recherche, UMR_S 1064, Institut National de la Santé et de la Recherche Médicale , Nantes , France ; Institut de Transplantation Urologie Néphrologie (ITUN), Université de Nantes , Nantes , France ; Effimune SAS , Nantes , France.
Gilles BlanchoUnité Mixte de Recherche, UMR_S 1064, Institut National de la Santé et de la Recherche Médicale , Nantes , France ; Institut de Transplantation Urologie Néphrologie (ITUN), Université de Nantes , Nantes , France.
Bernard VanhoveUnité Mixte de Recherche, UMR_S 1064, Institut National de la Santé et de la Recherche Médicale , Nantes , France ; Institut de Transplantation Urologie Néphrologie (ITUN), Université de Nantes , Nantes , France ; Effimune SAS , Nantes , France.
Institut de Transplantation Urologie en Nephrologie · FRNantes Université · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CD28 and CTLA-4 are prototypal co-stimulatory and co-inhibitory cell surface signaling molecules interacting with CD80/86, known to be critical for immune response initiation and regulation, respectively. Initial "bench-to-beside" translation, two decades ago, resulted in the development of CTLA4-Ig, a biologic that targets CD80/86 and prevents T-cell costimulation. In spite of its proven effectiveness in inhibiting allo-immune responses, particularly in murine models, clinical experience in kidney transplantation with belatacept (high-affinity CTLA4-Ig molecule) reveals a high incidence of acute, cell-mediated rejection. Originally, the etiology of belatacept-resistant graft rejection was thought to be heterologous immunity, i.e., the cross-reactivity of the pool of memory T cells from pathogen-specific immune responses with alloantigens. Recently, the standard view that memory T cells arise from effector cells after clonal contraction has been challenged by a "developmental" model, in which less differentiated memory T cells generate effector cells. This review delineates how this shift in paradigm, given the differences in co-stimulatory and co-inhibitory signal depending on the maturation stage, could profoundly affect our understanding of the CD28/CD80-86/CTLA-4 blockade and highlights the potential advantages of selectively targeting CD28, instead of CD80/86, to control post-transplant immune responses.

Indexed as

CD28costimulation blockadeCTLA-4CTLA4-Igeffector T cellheterologous immunitymemory T celltransplantation immunology

Identifiers

PMID26322044
PMCPMC4532816
OpenAlexW1559425537

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.