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. 2025 Jan 10;15:1580. doi: 10.1038/s41598-025-85452-x

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© The Author(s) 2025

Open Access This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, 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 you modified the licensed material. You do not have permission under this licence to share adapted material derived from this article or parts of it. 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-nc-nd/4.0/.

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Fig. 1 — Strategy for gating of ILCs in CB and placenta samples using flow cytometry. (A and B) ILCs were sorted into three subgroups: ILC1, Lin⁻CD127⁺c-Kit⁻CRTH2⁻; ILC2, Lin⁻CD127⁺CRTH2⁺; ILC3, Lin⁻CD127⁺c-Kit⁺CRTH2⁻ (FMO staining of PBMCs and placental tissue is shown in supplementary Fig. 1 and supplementary Fig. 2, respectively). (C and D) As Arg1 expression is thought to be responsible for the activity and function of ILC2s, the percentage of ILC1s, ILC2s, and Arg1⁺ILC2s was evaluated in the CB and placenta samples. CB, cord blood; GDM, gestational diabetes mellitus; CG, control group; * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001.