ArticleThe Journal of experimental medicine2013
Cytotoxic T cells induce proliferation of chronic myeloid leukemia stem cells by secreting interferon-γ.
Article in The Journal of experimental medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 79 citations in OpenAlex.
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- Effects of the STAMP-inhibitor asciminib on T cell activation and metabolic fitness compared to tyrosine kinase inhibition by imatinib, dasatinib, and nilotinib.Cancer immunology, immunotherapy : CII · 2023Article
- Progress of research on PD-1/PD-L1 in leukemia.Frontiers in immunology · 2023Review
- Tumor microenvironment enriches the stemness features: the architectural event of therapy resistance and metastasis.Molecular cancer · 2022Review
- Splenic red pulp macrophages provide a niche for CML stem cells and induce therapy resistance.Leukemia · 2022Article
- IFNγ directly counteracts imatinib-induced apoptosis of primary human CD34+ CML stem/progenitor cells potentially through the upregulation of multiple key survival factors.Oncoimmunology · 2022Article
- Mechanism underlying the immune checkpoint inhibitor-induced hyper-progressive state of cancer.Cancer drug resistance (Alhambra, Calif.) · 2022Review
- Interferon-gamma inhibits aldehyde dehydrogenasebright cancer stem cells in the 4T1 mouse model of breast cancer.Chinese medical journal · 2021Article
- Tnfrsf4-expressing regulatory T cells promote immune escape of chronic myeloid leukemia stem cells.JCI insight · 2021Article
- From the niche to malignant hematopoiesis and back: reciprocal interactions between leukemia and the bone marrow microenvironment.JBMR plus · 2021Article
- Stem Cells and Cancer Stem Cells: The Jekyll and Hyde Scenario and Their Implications in Stem Cell Therapy.Biomedicines · 2021Review
- Personalized Immunotherapy Treatment Strategies for a Dynamical System of Chronic Myelogenous Leukemia.Cancers · 2021Article
- Yin and Yang: The dual effects of interferons on hematopoiesis.Experimental hematology · 2021Review
- The tumor-promoting effects of the adaptive immune system: a cause of hyperprogressive disease in cancer?Cellular and molecular life sciences : CMLS · 2021Review
- Interferons in cancer immunoediting: sculpting metastasis and immunotherapy response.The Journal of clinical investigation · 2021Review
- Combination Therapies in Chronic Myeloid Leukemia for Potential Treatment-Free Remission: Focus on Leukemia Stem Cells and Immune Modulation.Frontiers in oncology · 2021Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic myeloid leukemia (CML) is a clonal myeloproliferative neoplasia arising from the oncogenic break point cluster region/Abelson murine leukemia viral oncogene homolog 1 translocation in hematopoietic stem cells (HSCs), resulting in a leukemia stem cell (LSC). Curing CML depends on the eradication of LSCs. Unfortunately, LSCs are resistant to current treatment strategies. The host's immune system is thought to contribute to disease control, and several immunotherapy strategies are under investigation. However, the interaction of the immune system with LSCs is poorly defined. In the present study, we use a murine CML model to show that LSCs express major histocompatibility complex (MHC) and co-stimulatory molecules and are recognized and killed by leukemia-specific CD8(+) effector CTLs in vitro. In contrast, therapeutic infusions of effector CTLs into CML mice in vivo failed to eradicate LSCs but, paradoxically, increased LSC numbers. LSC proliferation and differentiation was induced by CTL-secreted IFN-γ. Effector CTLs were only able to eliminate LSCs in a situation with minimal leukemia load where CTL-secreted IFN-γ levels were low. In addition, IFN-γ increased proliferation and colony formation of CD34(+) stem/progenitor cells from CML patients in vitro. Our study reveals a novel mechanism by which the immune system contributes to leukemia progression and may be important to improve T cell-based immunotherapy against leukemia.
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