Immune‐dysregulation harnessing in myeloid neoplasms

Abstract Myeloid malignancies arise in bone marrow microenvironments and shape these microenvironments in favor of malignant development. Immune suppression is one of the most important stages in myeloid leukemia progression. Leukemic clone expansion and immune dysregulation occur simultaneously in...

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Main Authors: Mohammad Jafar Sharifi, Ling Xu, Nahid Nasiri, Mehnoosh Ashja‐Arvan, Hadis Soleimanzadeh, Mazdak Ganjalikhani‐Hakemi
Format: Article
Language:English
Published: Wiley 2024-09-01
Series:Cancer Medicine
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Online Access:https://doi.org/10.1002/cam4.70152
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author Mohammad Jafar Sharifi
Ling Xu
Nahid Nasiri
Mehnoosh Ashja‐Arvan
Hadis Soleimanzadeh
Mazdak Ganjalikhani‐Hakemi
author_facet Mohammad Jafar Sharifi
Ling Xu
Nahid Nasiri
Mehnoosh Ashja‐Arvan
Hadis Soleimanzadeh
Mazdak Ganjalikhani‐Hakemi
author_sort Mohammad Jafar Sharifi
collection DOAJ
description Abstract Myeloid malignancies arise in bone marrow microenvironments and shape these microenvironments in favor of malignant development. Immune suppression is one of the most important stages in myeloid leukemia progression. Leukemic clone expansion and immune dysregulation occur simultaneously in bone marrow microenvironments. Complex interactions emerge between normal immune system elements and leukemic clones in the bone marrow. In recent years, researchers have identified several of these pathological interactions. For instance, recent works shows that the secretion of inflammatory cytokines such as tumor necrosis factor‐α (TNF‐α), from bone marrow stromal cells contributes to immune dysregulation and the selective proliferation of JAK2V617F+ clones in myeloproliferative neoplasms. Moreover, inflammasome activation and sterile inflammation result in inflamed microenvironments and the development of myelodysplastic syndromes. Additional immune dysregulations, such as exhaustion of T and NK cells, an increase in regulatory T cells, and impairments in antigen presentation are common findings in myeloid malignancies. In this review, we discuss the role of altered bone marrow microenvironments in the induction of immune dysregulations that accompany myeloid malignancies. We also consider both current and novel therapeutic strategies to restore normal immune system function in the context of myeloid malignancies.
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spelling doaj-art-017af456b7084544899aebf49d46513c2025-02-07T09:08:08ZengWileyCancer Medicine2045-76342024-09-011317n/an/a10.1002/cam4.70152Immune‐dysregulation harnessing in myeloid neoplasmsMohammad Jafar Sharifi0Ling Xu1Nahid Nasiri2Mehnoosh Ashja‐Arvan3Hadis Soleimanzadeh4Mazdak Ganjalikhani‐Hakemi5Division of Laboratory Hematology and Blood Banking, Department of Medical Laboratory Sciences, School of Paramedical Sciences Shiraz University of Medical Sciences Shiraz IranInstitute of Hematology, School of Medicine, Key Laboratory for Regenerative Medicine of Ministry of Education, Jinan University Guangzhou ChinaDivision of Laboratory Hematology and Blood Banking, Department of Medical Laboratory Sciences, School of Paramedical Sciences Shiraz University of Medical Sciences Shiraz IranRegenerative and Restorative Medicine Research Center (REMER) Research Institute of Health sciences and Technology (SABITA), Istanbul Medipol University Istanbul TurkeyDivision of Laboratory Hematology and Blood Banking, Department of Medical Laboratory Sciences, School of Paramedical Sciences Shiraz University of Medical Sciences Shiraz IranRegenerative and Restorative Medicine Research Center (REMER) Research Institute of Health sciences and Technology (SABITA), Istanbul Medipol University Istanbul TurkeyAbstract Myeloid malignancies arise in bone marrow microenvironments and shape these microenvironments in favor of malignant development. Immune suppression is one of the most important stages in myeloid leukemia progression. Leukemic clone expansion and immune dysregulation occur simultaneously in bone marrow microenvironments. Complex interactions emerge between normal immune system elements and leukemic clones in the bone marrow. In recent years, researchers have identified several of these pathological interactions. For instance, recent works shows that the secretion of inflammatory cytokines such as tumor necrosis factor‐α (TNF‐α), from bone marrow stromal cells contributes to immune dysregulation and the selective proliferation of JAK2V617F+ clones in myeloproliferative neoplasms. Moreover, inflammasome activation and sterile inflammation result in inflamed microenvironments and the development of myelodysplastic syndromes. Additional immune dysregulations, such as exhaustion of T and NK cells, an increase in regulatory T cells, and impairments in antigen presentation are common findings in myeloid malignancies. In this review, we discuss the role of altered bone marrow microenvironments in the induction of immune dysregulations that accompany myeloid malignancies. We also consider both current and novel therapeutic strategies to restore normal immune system function in the context of myeloid malignancies.https://doi.org/10.1002/cam4.70152acute myeloid leukemiamyelodysplastic syndromemyeloproliferative disorderstumor‐infiltrating immune cells
spellingShingle Mohammad Jafar Sharifi
Ling Xu
Nahid Nasiri
Mehnoosh Ashja‐Arvan
Hadis Soleimanzadeh
Mazdak Ganjalikhani‐Hakemi
Immune‐dysregulation harnessing in myeloid neoplasms
Cancer Medicine
acute myeloid leukemia
myelodysplastic syndrome
myeloproliferative disorders
tumor‐infiltrating immune cells
title Immune‐dysregulation harnessing in myeloid neoplasms
title_full Immune‐dysregulation harnessing in myeloid neoplasms
title_fullStr Immune‐dysregulation harnessing in myeloid neoplasms
title_full_unstemmed Immune‐dysregulation harnessing in myeloid neoplasms
title_short Immune‐dysregulation harnessing in myeloid neoplasms
title_sort immune dysregulation harnessing in myeloid neoplasms
topic acute myeloid leukemia
myelodysplastic syndrome
myeloproliferative disorders
tumor‐infiltrating immune cells
url https://doi.org/10.1002/cam4.70152
work_keys_str_mv AT mohammadjafarsharifi immunedysregulationharnessinginmyeloidneoplasms
AT lingxu immunedysregulationharnessinginmyeloidneoplasms
AT nahidnasiri immunedysregulationharnessinginmyeloidneoplasms
AT mehnooshashjaarvan immunedysregulationharnessinginmyeloidneoplasms
AT hadissoleimanzadeh immunedysregulationharnessinginmyeloidneoplasms
AT mazdakganjalikhanihakemi immunedysregulationharnessinginmyeloidneoplasms