ArticleJCI insight2025
NKG2D blockade impairs tissue-resident memory T cell accumulation and reduces chronic lung allograft dysfunction.
Article in JCI insight, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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.
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.
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Who cites it
8 citing papers in PubMed.
- Targeting the CD4Molecular biomedicine · 2026Article
- Lung transplantation in 2025: a narrative review of progress, challenges, and the road ahead.Journal of thoracic disease · 2026Review
- Immunogenomic landscape of the T cell repertoire after human lung transplantation and its clinical relevance.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2026Article
- Tissue-resident memory T cells in organ transplantation: implications for immune homeostasis and graft outcomes.Inflammation and regeneration · 2026Review
- The Myeloid-T Lymphocyte Axis in Chronic Lung Allograft Rejection: Emerging Insights into the Immune Circuitry Driving Fibrosis.Results and problems in cell differentiation · 2026Review
- Single-cell analysis indicating CCR8 modulates CD8Scientific reports · 2025Article
- Revisiting co-stimulation blockade in lung transplantation: Insights from a RAS-type CLAD mouse model.The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation · 2025Article
- The search for peripheral tolerance in lung transplantation.Current opinion in pulmonary medicine · 2025Review
Corrections and comments
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Authors and funding
19 authors.
Funding
Abstract
Chronic lung allograft dysfunction (CLAD) substantially limits long-term survival following lung transplantation. To identify potential targets for CLAD prevention, T cells from explanted CLAD lungs and lung-draining lymph nodes, as well as diseased and nondiseased controls were isolated and single-cell RNA sequencing and TCR sequencing were performed. TCR sequencing revealed a clonally expanded population of CD8+ tissue-resident memory T cells (TRMs) with high cytotoxic potential, including upregulation of KLRK1, encoding the co-receptor NKG2D. These cytotoxic CD8+ TRMs accumulated around the CLAD airways and had a 100-fold increase in clonal overlap with lung-draining lymph nodes when compared with non-CLAD lungs. Using a murine model of orthotopic lung transplantation, we confirmed that cytotoxic CD8+ TRM accumulation was due to chronic rejection and not transplantation alone. Furthermore, blocking NKG2D in vivo attenuated the airway remodeling following transplantation and diminished airway accumulation of CD8+ T cells. Our findings support NKG2D as a potential therapeutic target for CLAD, affecting cytotoxic CD8+ TRM accumulation.
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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 OpenQuestion graph.