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. 2022 Sep 28;13:1000996. doi: 10.3389/fimmu.2022.1000996

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Copyright © 2022 Luciano, Krenn and Horejs-Hoeck

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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Cytokines supporting AML progression. Osteoblasts, myeloblasts and mesenchymal stromal cells (MSCs) secrete osteopontin. This in turn promotes AML cell proliferation and disease progression. CXCL12 is mainly secreted by perivascular stromal cells (PSCs), and osteoblasts and promotes growth and survival of AML blasts cell via the chemokine receptor CXCR4. IL-1β acts on myeloblasts and HSPCs, which express the IL-1 receptor (IL-1R) as well as the IL-1 receptor accessor protein (IL-1RAP), thereby enhancing IL-1β production, AML cell proliferation and survival. IL-1 signaling can be blocked by Canakinumab, a human monoclonal antibody targeting IL-1β. IL-8 is constitutively produced by AML myeloblasts and acts in an autocrine way. MSCs and myeloblasts are potent sources of IL-6, which can be blocked by IL-6-blocking antibodies such as Siltuximab. Created with Biorender.com.