Bone Marrow Immune Microenvironment in Myelodysplastic Syndromes

The BM, the major hematopoietic organ in humans, consists of a pleiomorphic environment of cellular, extracellular, and bioactive compounds with continuous and complex interactions between them, leading to the formation of mature blood cells found in the peripheral circulation. Systemic and local in...

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Main Authors: Olga Kouroukli, Argiris Symeonidis, Periklis Foukas, Myrto-Kalliopi Maragkou, Eleni P. Kourea
Format: Article
Language:English
Published: MDPI AG 2022-11-01
Series:Cancers
Subjects:
Online Access:https://www.mdpi.com/2072-6694/14/22/5656
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author Olga Kouroukli
Argiris Symeonidis
Periklis Foukas
Myrto-Kalliopi Maragkou
Eleni P. Kourea
author_facet Olga Kouroukli
Argiris Symeonidis
Periklis Foukas
Myrto-Kalliopi Maragkou
Eleni P. Kourea
author_sort Olga Kouroukli
collection DOAJ
description The BM, the major hematopoietic organ in humans, consists of a pleiomorphic environment of cellular, extracellular, and bioactive compounds with continuous and complex interactions between them, leading to the formation of mature blood cells found in the peripheral circulation. Systemic and local inflammation in the BM elicit stress hematopoiesis and drive hematopoietic stem cells (HSCs) out of their quiescent state, as part of a protective pathophysiologic process. However, sustained chronic inflammation impairs HSC function, favors mutagenesis, and predisposes the development of hematologic malignancies, such as myelodysplastic syndromes (MDS). Apart from intrinsic cellular mechanisms, various extrinsic factors of the BM immune microenvironment (IME) emerge as potential determinants of disease initiation and evolution. In MDS, the IME is reprogrammed, initially to prevent the development, but ultimately to support and provide a survival advantage to the dysplastic clone. Specific cellular elements, such as myeloid-derived suppressor cells (MDSCs) are recruited to support and enhance clonal expansion. The immune-mediated inhibition of normal hematopoiesis contributes to peripheral cytopenias of MDS patients, while immunosuppression in late-stage MDS enables immune evasion and disease progression towards acute myeloid leukemia (AML). In this review, we aim to elucidate the role of the mediators of immune response in the initial pathogenesis of MDS and the evolution of the disease.
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spelling doaj.art-206ce6d29e57492997c71e4b886e504d2023-11-24T07:54:38ZengMDPI AGCancers2072-66942022-11-011422565610.3390/cancers14225656Bone Marrow Immune Microenvironment in Myelodysplastic SyndromesOlga Kouroukli0Argiris Symeonidis1Periklis Foukas2Myrto-Kalliopi Maragkou3Eleni P. Kourea4Department of Pathology, University Hospital of Patras, 26504 Patras, GreeceHematology Division, Department of Internal Medicine, School of Medicine, University of Patras, 26332 Patras, Greece2nd Department of Pathology, Attikon University Hospital, Medical School, National and Kapodistrian University of Athens, 12462 Athens, GreeceDepartment of Nutritional Sciences and Dietetics, School of Health Sciences, International Hellenic University, 54124 Thessaloniki, GreeceDepartment of Pathology, School of Medicine, University of Patras, 26504 Patras, GreeceThe BM, the major hematopoietic organ in humans, consists of a pleiomorphic environment of cellular, extracellular, and bioactive compounds with continuous and complex interactions between them, leading to the formation of mature blood cells found in the peripheral circulation. Systemic and local inflammation in the BM elicit stress hematopoiesis and drive hematopoietic stem cells (HSCs) out of their quiescent state, as part of a protective pathophysiologic process. However, sustained chronic inflammation impairs HSC function, favors mutagenesis, and predisposes the development of hematologic malignancies, such as myelodysplastic syndromes (MDS). Apart from intrinsic cellular mechanisms, various extrinsic factors of the BM immune microenvironment (IME) emerge as potential determinants of disease initiation and evolution. In MDS, the IME is reprogrammed, initially to prevent the development, but ultimately to support and provide a survival advantage to the dysplastic clone. Specific cellular elements, such as myeloid-derived suppressor cells (MDSCs) are recruited to support and enhance clonal expansion. The immune-mediated inhibition of normal hematopoiesis contributes to peripheral cytopenias of MDS patients, while immunosuppression in late-stage MDS enables immune evasion and disease progression towards acute myeloid leukemia (AML). In this review, we aim to elucidate the role of the mediators of immune response in the initial pathogenesis of MDS and the evolution of the disease.https://www.mdpi.com/2072-6694/14/22/5656MDSBMmicroenvironmentHSC nichepathogenesisinflamm-aging
spellingShingle Olga Kouroukli
Argiris Symeonidis
Periklis Foukas
Myrto-Kalliopi Maragkou
Eleni P. Kourea
Bone Marrow Immune Microenvironment in Myelodysplastic Syndromes
Cancers
MDS
BM
microenvironment
HSC niche
pathogenesis
inflamm-aging
title Bone Marrow Immune Microenvironment in Myelodysplastic Syndromes
title_full Bone Marrow Immune Microenvironment in Myelodysplastic Syndromes
title_fullStr Bone Marrow Immune Microenvironment in Myelodysplastic Syndromes
title_full_unstemmed Bone Marrow Immune Microenvironment in Myelodysplastic Syndromes
title_short Bone Marrow Immune Microenvironment in Myelodysplastic Syndromes
title_sort bone marrow immune microenvironment in myelodysplastic syndromes
topic MDS
BM
microenvironment
HSC niche
pathogenesis
inflamm-aging
url https://www.mdpi.com/2072-6694/14/22/5656
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AT argirissymeonidis bonemarrowimmunemicroenvironmentinmyelodysplasticsyndromes
AT periklisfoukas bonemarrowimmunemicroenvironmentinmyelodysplasticsyndromes
AT myrtokalliopimaragkou bonemarrowimmunemicroenvironmentinmyelodysplasticsyndromes
AT elenipkourea bonemarrowimmunemicroenvironmentinmyelodysplasticsyndromes