ArticleScientific reports2022
The CD226/TIGIT axis is involved in T cell hypo-responsiveness appearance in long-term kidney transplant recipients.
Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 7 citations in OpenAlex.
- Allospecific splenic Tr1 cells drive effector T cell exhaustion through up-regulated Areg-EGFR signaling to promote transplant tolerance.Science advances · 2026Article
- TIGITFrontiers in immunology · 2026Review
- T cell Activation Marker HLA-DR Reflects Tacrolimus-Associated Immunosuppressive Burden and BK Viremia Risk After Kidney Transplantation - An Observational Cohort Study.Transplant international : official journal of the European Society for Organ Transplantation · 2025Observational
- SARS-CoV-2-specific immune responses converge in kidney disease patients and controls with hybrid immunity.NPJ vaccines · 2024Article
- Exhaustion of T cells after renal transplantation.Frontiers in immunology · 2024Review
- Immune Checkpoints in Solid Organ Transplantation.Biology · 2023Review
- Immune-checkpoint expression in antigen-presenting cells (APCs) of cytomegaloviruses infection after transplantation: as a diagnostic biomarker.Archives of microbiology · 2023Review
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
T cell exhaustion refers to a dysfunctional state in which effector T cells present a decreased ability to proliferate and to produce cytokines, while the co-expression of inhibitory receptors increases. We investigated global and donor-specific T cell responses in a cohort of stable, living-donor kidney transplant patients that received similar immunosuppression. After transplantation, an increase in the ratio of TIGIT + /CD226 + in mCD4 + T cells (r = 0.47, p = 0.01), and a decrease of CD226 + TIGIT-mCD4 + T cells was observed (r = - 0.55, p = 0.001). This leads to an increase of dysfunctional T cells in patients far from transplantation. In mCD8 + T cells, a decrease of IL-2 production after mitogenic stimulation was observed far from transplantation. Phenotypic analyses revealed an increase of mCD8 + T cells co-expressing PD-1 and TIGIT over time (r = 0.51, p = 0.02). After donor-specific stimulation, the ability of CD4 + T cells to proliferate was decreased compared with third parties. CD4 + T cells expressing CD226 and TIGIT were correlated with allospecific CD4 + proliferation (r = 0.68, p = 0.04). Our study suggests that after kidney transplantation a T cell hyporesponsiveness appears over time, driven by a dysregulation of CD226/TIGIT axis in mCD4 + T cells, associated with an increase of PD1 + TIGIT + in mCD8 + T cells.
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