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Immune-Dysregulation Harnessing in Myeloid Neoplasms Publisher Pubmed



Sharifi MJ1 ; Xu L2 ; Nasiri N1 ; Ashjaarvan M3 ; Soleimanzadeh H1 ; Ganjalikhanihakemi M3, 4
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Authors Affiliations
  1. 1. Division of Laboratory Hematology and Blood Banking, Department of Medical Laboratory Sciences, School of Paramedical Sciences, Shiraz University of Medical Sciences, Shiraz, Iran
  2. 2. Institute of Hematology, School of Medicine, Key Laboratory for Regenerative Medicine of Ministry of Education, Jinan University, Guangzhou, China
  3. 3. Regenerative and Restorative Medicine Research Center (REMER), Research Institute of Health sciences and Technology (SABITA), Istanbul Medipol University, Istanbul, Turkey
  4. 4. Department of Immunology, Faculty of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran

Source: Cancer Medicine Published:2024


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. © 2024 The Author(s). Cancer Medicine published by John Wiley & Sons Ltd.
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