ArticleJCI insight2018
Signatures of CD8+ T cell dysfunction in AML patients and their reversibility with response to chemotherapy.
Article in JCI insight, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 134 papers.
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Who cites it
134 citing papers in PubMed, 210 citations in OpenAlex.
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- Azacitidine-induced reconstitution of the bone marrow T cell repertoire is associated with superior survival in AML patients.Blood cancer journal · 2022Trial
- Phase II Trial of Pembrolizumab after High-Dose Cytarabine in Relapsed/Refractory Acute Myeloid Leukemia.Blood cancer discovery · 2021Trial
- Remodeling memory T cells with chemotherapy and immune checkpoint inhibitors as host pre-conditioning to empower in vivo CAR-T therapy.Synthetic and systems biotechnology · 2026Review
- FGF18 mediates fibroblast-leukemia cross talk to promote acute myeloid leukemia progression.Blood · 2026Article
- Review
- Clinical implications of RAS mutations in AML: prognostic significance is based upon the involved gene and mutation complexity.Blood advances · 2026Article
- T-cell miR-155 regulates the response to tumor-specific mRNA vaccines in a murine model of acute myeloid leukemia.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- P2X7 receptor: An emerging therapeutic target in acute myeloid leukemia (Review).International journal of oncology · 2026Review
- Azacytidine restores T cell function in AML by modulating DNA methylation.bioRxiv : the preprint server for biology · 2026Article
- CD8Science China. Life sciences · 2026Review
- Measurable residual disease testing in acute myeloid leukemia: current state, foundational models, and tools for future development.Cancer metastasis reviews · 2026Review
- Mechanistic basis and therapeutic modulation of T cell fitness to enhance CAR-T cell efficacy in hematological malignancies.Frontiers in immunology · 2026Review
- Article
- Microbiome dysbiosis and chemotherapy resistance in acute myeloid leukemia (AML).NPJ biofilms and microbiomes · 2025Review
- Aberrant expression of SLAMF6 constitutes a targetable immune escape mechanism in acute myeloid leukemia.Nature cancer · 2025Article
- B cell maturation antigen is a novel target for immunotherapy of acute myeloid leukemia.Journal of hematology & oncology · 2025Article
- CD123-targeting immunotherapeutic approaches in acute myeloid leukaemia.British journal of haematology · 2025Review
- Donor-Derived Vγ9Vδ2 T Cells for Acute Myeloid Leukemia: A Promising "Off-the-Shelf" Immunotherapy Approach.Cancers · 2025Article
- ST2/IL-33 axis blockade inhibits regulatory T cell cytotoxicity towards CD8 T cells in the leukemic niche.Nature communications · 2025Article
74 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
12 authors at 6 institutions in 2 countries.
Funding
Abstract
backgroundOur understanding of phenotypic and functional signatures of CD8+ T cell dysfunction in acute myeloid leukemia (AML) is limited. Deciphering these deranged T cell functional states and how they are impacted by induction chemotherapy is essential for incorporation of novel immune-based strategies to restore and maintain antileukemia immunity.
methodsWe utilized high-dimensional immunophenotyping, gene expression, and functional studies to characterize peripheral blood and bone marrow CD8+ T cells in 72 AML patients at diagnosis and after induction chemotherapy.
resultsOur data suggest that multiple aspects of deranged T cell function are operative in AML at diagnosis, with exhaustion and senescence being the dominant processes. Following treatment, the phenotypic and transcriptional profile of CD8+ T cells diverged between responders and nonresponders. Response to therapy correlated with upregulation of costimulatory, and downregulation of apoptotic and inhibitory, T cell signaling pathways, indicative of restoration of T cell function. In functional studies, AML blasts directly altered CD8+ T cell viability, expansion, co-signaling and senescence marker expression. This CD8+ T cell dysfunction was in part reversible upon PD-1 blockade or OX40 costimulation in vitro.
conclusionOur findings highlight the uniqueness of AML in sculpting CD8+ T cell responses and the plasticity of their signatures upon chemotherapy response, providing a compelling rationale for integration of novel immunotherapies to augment antileukemia immunity.
fundingThis work was supported by the Leukemia & Lymphoma Society grant no. 6449-13; NIH grants UM1-CA186691 and R01-HL110907-01; the American Society for Blood and Marrow Transplantation New Investigator Award/Gabrielle's Angel Foundation; the Vienna Fund for Innovative Cancer Research; and by fellowships from the Wenner-Gren Foundation and the Swedish Society for Medical Research.
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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.