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. 2021 Jun 1;12:683401. doi: 10.3389/fimmu.2021.683401

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Copyright © 2021 Fisher, Fowles, Zhou and Oh

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Hematopoietic bone marrow niches disrupted in MPNs. (A, B) Bone marrow niches in healthy hematopoiesis. (A) The endosteal niche: HSPC reside in contact with the endosteum, composed of osteoblasts that release TPO, promoting HSC quiescence. CXCL12 secreted by CAR cells promotes HSPC stasis in the bone marrow, while mesenchymal stromal cells (MSC) secrete SCF and IL-6. (B) The perivascular niche: HSPC reside in contact with blood vessels (BV), which are also contacted by the CXCL12-secreting CAR cells. This niche, however, is more prone to HSPC circulation than the endosteal niche. Monocytes (Mono) and megakaryocytes (Mega) secrete cytokines active on HSPC. (C, D) Disruption of hematopoietic niches in MF. (C) In MF, MSCs are abundant but CAR cells are reduced. The endosteum can be disrupted, and MSCs can differentiate into fibrocytes and deposit collagen, disrupting blood vessels in the hematopoietic space. Consequently, HSPC become mobilized. (D) Monocytes and megakaryocytes become abundant in the MPN bone marrow, releasing cytokines including TNF and the fibrogenic TGFβ. Monocytes, as well as MSCs, can differentiate into fibrocytes (71).