36-PUB: Regulatory T Cell–Related Signaling Pathway Variants, Adipokine Profiles, and Clinical Characteristics in Gestational Diabetes Mellitus

Introduction and Objective: Regulatory T (Treg) cells play a key role in immune tolerance during pregnancy. Altered Treg function has been implicated in the pathogenesis of gestational diabetes mellitus (GDM), although the underlying mechanisms remain unclear. This study aimed to investigate the associations between genetic polymorphisms in regulatory T cell-related signaling pathway genes (FOXP3, STAT5B, and IL2RA), adipokine levels, and clinical characteristics in Thai pregnant women with GDM. Methods: This retrospective cohort study included 49 Thai pregnant women diagnosed with GDM. Genetic polymorphisms in FOXP3, STAT5B, and IL2RA were identified using whole-exome sequencing. Associations between single-nucleotide polymorphisms (SNPs), adipokine concentrations (adiponectin, NGAL, resistin, adipsin, and PAI-1), and clinical parameters were assessed using one-way ANOVA or the Kruskal-Wallis test, as appropriate. Statistical significance was defined as a p value <0.05. Results: In FOXP3, two missense variants, including rs17847095 (c.155G>T; p.Gly52Val), were predicted to have moderate functional impact, and rs17847095 was significantly associated with adipsin levels (p = 0.016). In STAT5B, the missense variant rs199645527 (c.280C>T; p.Leu94Phe) showed a moderate predicted impact, while rs397837160 demonstrated a trend toward pre-pregnancy weight (p = 0.053). In IL2RA, rs2274036 and rs942200 were significantly associated with adipsin levels (p = 0.004 and p = 0.011, respectively). Additionally, rs11256354 was associated with neonatal birth weight (p = 0.004), and rs2274036 was associated with gestational age (p = 0.049). Conclusion: This study suggests that genetic polymorphisms in Treg-related genes are associated with adipokine levels and clinical characteristics in GDM, providing insight into immune-related mechanisms underlying GDM pathophysiology. Disclosure N. Masuwan: None. S. Suthon: None. S. Innang: None. S. Songlilitchuwong: None. T. Narkdontri: None. N. Teerawattanapong: None. W. Tangjittipokin: None.