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. 2023 Apr 12;14:79. doi: 10.1186/s13287-023-03323-6

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© The Author(s) 2023

Open AccessThis 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. 1 — Phenotype and function of MSCs in healthy individuals and ITP patients. MSCs were involved in platelet production by interacting with immune cells, including ① inhibition of mDC maturation; ② regulation of the ratio of T lymphocyte subsets; ③ inhibition of lymphocyte proliferation; ④ inhibition of antibody release from B cells; and ⑤ promotion of platelet production from megakaryocyte maturation. The function of ITP-MSCs was impaired, mainly by: ⑥ increased G0/G1 cells with restricted proliferation; ⑦ increased apoptosis; ⑧ decreased concentration of CXCL12, which may contribute to reduced ability of megakaryocytes to migrate from the bone marrow sinus to the blood sinus; ⑨ increased release of pro-inflammatory cytokines; ⑩ broad and flattened appearance; ⑪ increased apoptosis of MSCs due to complement deposition. Ps: copyright permission is not applicable