ArticleThe Journal of clinical investigation2017
Differential requirements for myeloid leukemia IFN-γ conditioning determine graft-versus-leukemia resistance and sensitivity.
Article in The Journal of clinical investigation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 25 citations in OpenAlex.
- SPHK1 deficiency promotes intestinal homeostasis by ameliorating ER stress-induced gastrointestinal injury during murine graft-versus-host disease.Science China. Life sciences · 2026Article
- IFN-γ and donor leukocyte infusions for relapsed myeloblastic malignancies after allogeneic hematopoietic stem cell transplantation.JCI insight · 2025Article
- Chemokine receptors are required for effector T-cell trafficking to GVHD tissues but not to bone marrow.Blood advances · 2025Article
- Lysosomal acid lipase A modulates leukemia stem cell response to venetoclax/tyrosine kinase inhibitor combination therapy in blast phase chronic myeloid leukemia.Haematologica · 2025Article
- Article
- Maintenance strategies for relapse prevention and treatment.Hematology. American Society of Hematology. Education Program · 2024Review
- The graft versus leukemia effect: donor lymphocyte infusions and cellular therapy.Frontiers in immunology · 2024Review
- Leukemia relapse via genetic immune escape after allogeneic hematopoietic cell transplantation.Nature communications · 2023Article
- Article
- Leukemia relapse via genetic immune escape after allogeneic hematopoietic cell transplantation.Research square · 2023Article
- From drug repositioning to target repositioning: prediction of therapeutic targets using genetically perturbed transcriptomic signatures.Bioinformatics (Oxford, England) · 2022Article
- Integrated Multiomic Profiling Identifies the Epigenetic Regulator PRC2 as a Therapeutic Target to Counteract Leukemia Immune Escape and Relapse.Cancer discovery · 2022Article
- USP22 deficiency in melanoma mediates resistance to T cells through IFNγ-JAK1-STAT1 signal axis.Molecular therapy : the journal of the American Society of Gene Therapy · 2021Article
- Dynamic immune profiling identifies the stronger graft-versus-leukemia (GVL) effects with haploidentical allografts compared to HLA-matched stem cell transplantation.Cellular & molecular immunology · 2021Article
- ATG5-Dependent Autophagy Uncouples T-cell Proliferative and Effector Functions and Separates Graft-versus-Host Disease from Graft-versus-Leukemia.Cancer research · 2021Article
- Biology of Disease Relapse in Myeloid Disease: Implication for Strategies to Prevent and Treat Disease Relapse After Stem-Cell Transplantation.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2021Review
- Granzyme A-producing T helper cells are critical for acute graft-versus-host disease.JCI insight · 2020Article
- T cell exhaustion and a failure in antigen presentation drive resistance to the graft-versus-leukemia effect.Nature communications · 2020Article
- Dissecting the biology of allogeneic HSCT to enhance the GvT effect whilst minimizing GvHD.Nature reviews. Clinical oncology · 2020Review
- H60: A Unique Murine Hematopoietic Cell-Restricted Minor Histocompatibility Antigen for Graft-versus-Leukemia Effect.Frontiers in immunology · 2020Review
Corrections and comments
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Authors and funding
7 authors at 5 institutions in 1 country.
Funding
Abstract
The graft-versus-leukemia (GVL) effect in allogeneic hematopoietic stem cell transplantation (alloSCT) is potent against chronic phase chronic myelogenous leukemia (CP-CML), but blast crisis CML (BC-CML) and acute myeloid leukemias (AML) are GVL resistant. To understand GVL resistance, we studied GVL against mouse models of CP-CML, BC-CML, and AML generated by the transduction of mouse BM with fusion cDNAs derived from human leukemias. Prior work has shown that CD4+ T cell-mediated GVL against CP-CML and BC-CML required intact leukemia MHCII; however, stem cells from both leukemias were MHCII negative. Here, we show that CP-CML, BC-CML, and AML stem cells upregulate MHCII in alloSCT recipients. Using gene-deficient leukemias, we determined that BC-CML and AML MHC upregulation required IFN-γ stimulation, whereas CP-CML MHC upregulation was independent of both the IFN-γ receptor (IFN-γR) and the IFN-α/β receptor IFNAR1. Importantly, IFN-γR-deficient BC-CML and AML were completely resistant to CD4- and CD8-mediated GVL, whereas IFN-γR/IFNAR1 double-deficient CP-CML was fully GVL sensitive. Mouse AML and BC-CML stem cells were MHCI+ without IFN-γ stimulation, suggesting that IFN-γ sensitizes these leukemias to T cell killing by mechanisms other than MHC upregulation. Our studies identify the requirement of IFN-γ stimulation as a mechanism for BC-CML and AML GVL resistance, whereas independence from IFN-γ renders CP-CML more GVL sensitive, even with a lower-level alloimmune response.
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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.