Supplementary material to "Glutamine metabolism shapes the phenotypic adaptation of uterine dendritic cells in response to early allogeneic pregnancy"

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true 3.1 UHH.FDR 10.25592/uhhfdm.18805 Thiele, Kristin 0000-0002-9343-9834 Division for Experimental Feto-Maternal Medicine, Department of Obstetrics and Fetal Medicine, Univer-sity Medical Center Hamburg-Eppendorf, Hamburg, Germany Diao, Lianghui 0000-0002-1159-9261 Shenzhen Key Laboratory for Reproductive Immunology of Peri-implantation, Shenzhen Zhongshan Insti-tute for Reproduction and Genetics, Fertility Center, Shenzhen Zhongshan Obstetrics & Gynecology Hospital, Shenzhen, China Supplementary material to "Glutamine metabolism shapes the phenotypic adaptation of uterine dendritic cells in response to early allogeneic pregnancy" Universität Hamburg 2026 Allogeneic pregnancy Dendritic cells Glutamine Immunometabolism Pregnancy hormones 2026-04-16 https://www.fdr.uni-hamburg.de/record/oai:fdr.uni-hamburg.de:18805 10.25592/uhhfdm.18542 2 Creative Commons Attribution Non Commercial Share Alike 4.0 International Open Access Supplementary material to "Glutamine metabolism shapes the phenotypic adaptation of uterine dendritic cells in response to early allogeneic pregnancy" published in American Journal of Physiology-Endocrinology and Metabolism, doi: 10.1152/ajpendo.00520.2025 ABSTRACT The impact of metabolic reprogramming on immune cell functions is increasingly recognized. However, it remains largely unexplored in terms of immune cells adaptation during reproduction. Dendritic cells (DC) are crucial for establishing and maintaining pregnancy by orchestrating maternal immune adaptation essential for embryo implantation and decidualization. Here, we characterized the phenotypic and metabolic characteristics of DCs during early pregnancy in an allogeneic mouse model and in response to the specific deletion of hormonal receptors on DCs. Frequency of uterine CD11c+ DCs on gestational day (gd) 7.5 remained equal to that of non-pregnant mice. However, we observed a functional shift from cDC1 to cDC2 in pregnant mice. In parallel, a metabolic switch in uterine DCs was identified by upregulation of genes representing fatty acid synthesis (Fasn, Acaca), fatty acid oxidation (Cpt1a), and glutamine-related metabolic pathways (Got2). The cell-specific deletion of the glucocorticoid receptor in DCs reduced their MHCII expression, accompanied by a reduction in Got2 expression. Glutamine deprivation in vitro dramatically reduced the absolute number of cultured bone marrow cells and the frequency of cDC1s while simultaneously increasing the frequency of cDC2s. Collectively, these findings establish glutamine metabolism as a key driver of DC adaptation during early pregnancy, revealing novel metabolic-immunological crosstalk at the maternal-fetal interface.