Evidence map›Paper›PMID 39479216›Full record

ReviewTransplant international : official journal of the European Society for Organ Transplantation2024

NK Cells: Not Just Followers But Also Initiators of Chronic Vascular Rejection.

Mathilde Chambon, Alice Koenig

Registry-linked trialAbstract readReview
In one paragraph

Review in Transplant international : official journal of the European Society for Organ Transplantation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07718308 (A Multicenter Exploratory Clinical Study of Targeted NK Cell Inhibition for Transplant Kidney Chronic Active Antibody-Mediated Rejection), which is not on this map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
–field-weighted citation impact
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.

NCT07718308 nanot yet recruitingnot on this mapstarted 2026, after this paper: background citation

A Multicenter Exploratory Clinical Study of Targeted NK Cell Inhibition for Transplant Kidney Chronic Active Antibody-Mediated Rejection (caABMR): Single Induction With CD38 Monoclonal Antibody Followed by Sequential Maintenance With Azathioprine

TypeinterventionalSponsorwujianyongRan2026 to 2028Enrolled20ConditionsKidney Transplantation, Antibody-mediated RejectionArmsCD38, Azathioprine (AZA), Standard Triple Immunosuppression Maintenance
3 · Its place in the literature

Who cites it

11 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Dual inhibition of mTOR and calcineurin pathways mitigates missing self-induced NK cell-mediated microvascular rejection.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  5. Article
  6. The Top 12 Most Impactful Papers in Clinical Transplantation in 2025: TI Editors' Choice.Transplant international : official journal of the European Society for Organ Transplantation · 2026
    Article
  7. Not all antibodies are created equal: total IgG glycosylation and severity of antibody-mediated rejection in kidney transplantation.Transplant international : official journal of the European Society for Organ Transplantation · 2026
    Article
  8. Article
  9. Antibody-mediated rejection-treatment standard.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2025
    Review
  10. Targeting CD38 in Antibody-Mediated Rejection.Transplant international : official journal of the European Society for Organ Transplantation · 2025
    Review
  11. Shedding Light on Microvascular Inflammation: Understanding Outcomes, But What Sparks the Flame?Transplant international : official journal of the European Society for Organ Transplantation · 2024
    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

2 authors.

Mathilde ChambonCIRI, INSERM U1111, Université Claude Bernard Lyon I, CNRS UMR5308, Ecole Normale Supérieure de Lyon, University of Lyon, Lyon, France.
Alice KoenigCIRI, INSERM U1111, Université Claude Bernard Lyon I, CNRS UMR5308, Ecole Normale Supérieure de Lyon, University of Lyon, Lyon, France.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic graft rejection represents a significant threat to long-term graft survival. Early diagnosis, understanding of the immunological mechanisms and appropriate therapeutic management are essential to improve graft survival and quality of life for transplant patients. Knowing which immune cells are responsible for chronic vascular rejection would allow us to provide effective and appropriate treatment for these patients. It is now widely accepted that natural killer (NK) cells play an important role in chronic vascular rejection. They can either initiate chronic vascular rejection by recognizing missing self on the graft or be recruited by donor-specific antibodies to destroy the graft during antibody-mediated rejection. Whatever the mechanisms of activation of NK cells, they need to be primed to become fully activated and damaging to the graft. A better understanding of the signaling pathways involved in NK cell priming and activation would pave the way for the development of new therapeutic strategies to cure chronic vascular rejection. This review examines the critical role of NK cells in the complex context of chronic vascular rejection.

Indexed as

Graft RejectionKiller Cells, NaturalAnimalsChronic DiseaseGraft SurvivalHumansantibody dependent cellular cytotoxicityantibody mediated rejectionchronic rejectionmissing selfnatural killer cells

Identifiers

PMID39479216
PMCPMC11521863

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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 Socratic graph.