WFRF:(Nordin Joel Z.)
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Extracellular vesicles originating from melanoma cells promote dysregulation in haematopoiesis as a component of cancer immunoediting
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- Mamand, Doste R. (författare)
- Karolinska Inst, Dept Lab Med, Biomol & Cellular Med BCM, Huddinge, Sweden.;Karolinska Inst, Karolinska Univ Hosp, Breast Ctr, Karolinska Comprehens Canc Ctr, Stockholm, Sweden.
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- Bazaz, Safa (författare)
- Karolinska Inst, Dept Lab Med, Biomol & Cellular Med BCM, Huddinge, Sweden.;Karolinska Univ Hosp Huddinge, Dept Cellular Therapy & Allogene Stem Cell Transpl, Stockholm, Sweden.;Karolinska Comprehens Canc Ctr, Stockholm, Sweden.
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- Mohammad, Dara K. (författare)
- Karolinska Inst, Ctr Hematol & Regenerat Med HERM, Dept Med Huddinge, Stockholm, Sweden.;Salahaddin Univ Erbil, Coll Agr Engn Sci, Erbil, Iraq.
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- Karolinska Inst, Dept Lab Med, Biomol & Cellular Med BCM, Huddinge, Sweden;Karolinska Inst, Karolinska Univ Hosp, Breast Ctr, Karolinska Comprehens Canc Ctr, Stockholm, Sweden. Karolinska Inst, Dept Lab Med, Biomol & Cellular Med BCM, Huddinge, Sweden.;Karolinska Univ Hosp Huddinge, Dept Cellular Therapy & Allogene Stem Cell Transpl, Stockholm, Sweden.;Karolinska Comprehens Canc Ctr, Stockholm, Sweden. (creator_code:org_t)
- Wiley, 2024
- 2024
- Engelska.
- Ingår i: Journal of Extracellular Vesicles. - : Wiley. - 2001-3078. ; 13:7
- Tidskriftsartikel (refereegranskat)
Abstract
Ämnesord
Stäng
- Haematopoiesis dysregulation with the presence of immature myeloid and erythroid immunosuppressive cells are key characteristics of the immune escape phase of tumour development. Here, the role of in vitro generated B16F10 tumour cell-derived extracellular vesicles (tEVs) as indirect cellular communicators, participating in tumour-induced dysregulation of haematopoiesis, was explored. The isolated tEVs displayed features of small EVs with a size range of 100-200 nm, expressed the common EV markers CD63, CD9, and Alix, and had a spherical shape with a lipid bilayer membrane. Proteomic profiling revealed significant levels of angiogenic factors, particularly vascular endothelial growth factor (VEGF), osteopontin, and tissue factor, associated with the tEVs. Systemic administration of these tEVs in syngeneic mice induced splenomegaly and disrupted haematopoiesis, leading to extramedullary haematopoiesis, expansion of splenic immature erythroid progenitors, reduced bone marrow cellularity, medullary expansion of granulocytic myeloid suppressor cells, and the development of anaemia. These effects closely mirrored those observed in tumour-bearing mice and were not seen after heat inactivating the tEVs. In vitro studies demonstrated that tEVs independently induced the expansion of bone marrow granulocytic myeloid suppressor cells and B cells while reducing the frequency of cells in the erythropoietic lineage. These effects of tEVs were significantly abrogated by the blockade of VEGF or heat inactivation. Our findings underscore the important role of tEVs in dysregulating haematopoiesis during the immune escape phase of cancer immunoediting, suggesting their potential as targets for addressing immune evasion and reinstating normal hematopoietic processes.
Ämnesord
- MEDICIN OCH HÄLSOVETENSKAP -- Medicinsk bioteknologi -- Medicinsk bioteknologi (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Medical Biotechnology -- Medical Biotechnology (hsv//eng)
Nyckelord
- angiogenesis factors
- erythroid progenitor cells (EPCs)
- immune escape
- immunosuppression
- MDSCs
- tEVs
- vascular endothelial growth factor
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- Mamand, Doste R.
- Bazaz, Safa
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- Liang, Xiuming
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- Mim, Carsten
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- Nordin, Joel Z.
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