• J. Korean Med. Sci. · Dec 2022

    Increased Pro-Inflammatory T Cells, Senescent T Cells, and Immune-Check Point Molecules in the Placentas of Patients With Gestational Diabetes Mellitus.

    • Yea Eun Kang, Hyon-Seung Yi, Min-Kyung Yeo, Jung Tae Kim, Danbit Park, Yewon Jung, Ok Soon Kim, Seong Eun Lee, Ji Min Kim, Kyong Hye Joung, Ju Hee Lee, Bon Jeong Ku, Mina Lee, and Hyun Jin Kim.
    • Division of Endocrinology and Metabolism, Department of Internal Medicine, Chungnam National University College of Medicine, Daejeon, Korea.
    • J. Korean Med. Sci. 2022 Dec 12; 37 (48): e338e338.

    BackgroundGestational diabetes mellitus (GDM) is the most common metabolic complication of pregnancy. To define the altered pathway in GDM placenta, we investigated the transcriptomic profiles from human placenta between GDM and controls.MethodsClinical parameters and postpartum complications were reviewed in all participants. Differentially expressed canonical pathways were analyzed between the GDM and control groups based on transcriptomic analysis. CD4+ T, CD8+ T, and senescent T cell subsets were determined by flow cytometry based on staining for specific intracellular cytokines.ResultsGene ontology analysis revealed that the placenta of GDM revealed upregulation of diverse mitochondria or DNA replication related pathways and downregulation of T-cell immunity related pathways. The maternal placenta of the GDM group had a higher proportion of CD4+ T and CD8+ T cells than the control group. Interestingly, senescent CD4+ T cells tended to increase and CD8+ T cells were significantly increased in GDM compared to controls, along with increased programmed cell death-1 (CD274+) expression. Programmed death-ligand 1 expression in syncytotrophoblasts was also significantly increased in patients with GDM.ConclusionThis study demonstrated increased proinflammatory T cells, senescent T cells and immune-check point molecules in GDM placentas, suggesting that changes in senescent T cells and immune-escape signaling might be related to the pathophysiology of GDM.© 2022 The Korean Academy of Medical Sciences.

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