The DOI matches its Crossref record; 34 of the 34 references it cites were found in a registry or an index.
Thermal- and Oxidative Stress Causes Enhanced Release of NKG2D Ligand-Bearing Immunosuppressive Exosomes in Leukemia/Lymphoma T and B Cells
Open accessAbstract
Immune evasion from NK surveillance related to inadequate NK-cell function has been suggested as an explanation of the high incidence of relapse and fatal outcome of many blood malignancies. In this report we have used Jurkat and Raji cell lines as a model for studies of the NKG2D receptor-ligand system in T-and B cell leukemia/lymphoma. Using real-time quantitative RT-PCR and immunoflow cytometry we show that Jurkat and Raji cells constitutively express mRNA and protein for the stress-inducible NKG2D ligands MICA/B and ULBP1 and 2, and up-regulate the expression in a cell-line specific and stress-specific manner. Furthermore, we revealed by electron microscopy, immunoflow cytometry and western blot that these ligands were expressed and secreted on exosomes, nanometer-sized microvesicles of endosomal origin. Acting as a decoy, the NKG2D ligand-bearing exosomes downregulate the in vitro NKG2D receptor-mediated cytotoxicity and thus impair NK-cell function. Interestingly, thermal and oxidative stress enhanced the exosome secretion generating more soluble NKG2D ligands that aggravated the impairment of the cytotoxic response. Taken together, our results might partly explain the clinically observed NK-cell dysfunction in patients suffering from leukemia/lymphoma. The adverse effect of thermal and oxidative stress, enhancing the release of immunosuppressive exosomes, should be considered when cytostatic and hyperthermal anti-cancer therapies are designed.
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Tumor-derived exosomes are a source of shared tumor rejection antigens for CTL cross-priming
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Tumour-derived soluble MIC ligands impair expression of NKG2D and T-cell activation
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Malignant effusions and immunogenic tumour-derived exosomes
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Exosomes: A Common Pathway for a Specialized Function
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NKG2D-deficient mice are defective in tumor surveillance in models of spontaneous malignancy
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Self-citationThe Role of the NKG2D Immunoreceptor in Immune Cell Activation and Natural Killing
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Cutting Edge: Down-Regulation of MICA on Human Tumors by Proteolytic Shedding
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Extracellular vesicles: biology and emerging therapeutic opportunities
EL Andaloussi, S., Mäger, I., Breakefield, X. O., & Wood, M. J. A. (2013) · Nature Reviews Drug Discovery · doi:10.1038/nrd3978 · Cited by 3,571
Classification, Functions, and Clinical Relevance of Extracellular Vesicles
van der Pol, E., Böing, A. N., Harrison, P., Sturk, A., & Nieuwland, R. (2012) · Pharmacological Reviews · doi:10.1124/pr.112.005983 · Cited by 1,754
Regulation of Ligands for the NKG2D Activating Receptor
Raulet, D. H., Gasser, S., Gowen, B. G., Deng, W., & Jung, H. (2013) · Annual Review of Immunology · doi:10.1146/annurev-immunol-032712-095951 · Cited by 848
Exosome-Based Cell-Cell Communication in the Tumor Microenvironment
Maia, J., Caja, S., Strano Moraes, M. C., Couto, N., & Costa-Silva, B. (2018) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2018.00018 · Cited by 666
Metadata
- Authors
- Hedlund, M., Nagaeva, O., Kargl, D., Baranov, V., & Mincheva-Nilsson, L.
- Venue
- PLoS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2011-02-25
- Volume
- 6
- Issue
- 2
- Pages
- e16899
- ISSN
- 1932-6203 (ISSN-L)
- OpenAlex
- W2020404158
- Cited by
- 360
- References
- 34
- FWCI
- 5.52
- Type
- journal article
- Language
- en
- Open access
- gold
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- CoChat. (2026). Citation check: Thermal- and Oxidative Stress Causes Enhanced Release of NKG2D Ligand-Bearing Immunosuppressive Exosomes in Leukemia/Lymphoma T and B Cells. https://app.cochat.ai/papers/10.1371/journal.pone.0016899
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- Hedlund, M., Nagaeva, O., Kargl, D., Baranov, V., & Mincheva-Nilsson, L. (2011). Thermal- and Oxidative Stress Causes Enhanced Release of NKG2D Ligand-Bearing Immunosuppressive Exosomes in Leukemia/Lymphoma T and B Cells. PLoS ONE. https://doi.org/10.1371/journal.pone.0016899
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.