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. 2023 Jul 6;16:71. doi: 10.1186/s13045-023-01473-x

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© The Author(s) 2023

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 3 — The regulatory mechanism of non-classical TAMCs. (1) Spleen EMH: Splenic CD11b⁺Gr-1^intLy6C^hi cells expand in the marginal zone of the spleen. Spleen recruits specific HSPCs subpopulation from BM via the CCL2/CCR2 axis, and HSPC differentiates into TAMCs driven by endogenous GM-CSF signals and splenic local education. The AngII-AGTR1A signaling pathway increases the retention of HSPCs in the spleen. (2) Tumors block the default red blood cell differentiation pathway of CD45⁺EPCs in the spleen. Under the effect of GM-CSF, CD45⁺EPCs trans-differentiate into EDMCs. (3) During embryogenesis, EMPs are formed in the yolk sac. TRMs are derived from both early wave and late wave EMPs. (4) Cancers use thymic stromal lymphopoietin and G-CSF to mobilize BM pre-B accumulation in the spleen. In tumor microenvironment, pre-B responds to cancer-secreted M-CSF and trans-differentiates into B-MF