Inflammatory biomarkers and immune dysregulation in gestational diabetes mellitus: emerging mechanisms and therapeutic prospects
Abstract
Gestational diabetes mellitus (GDM) is a common pregnancy-related metabolic disorder that increases the risk of adverse maternal and neonatal outcomes and predisposes both mothers and offspring to long-term metabolic disease. Beyond pregnancy-induced insulin resistance, accumulating evidence indicates that GDM is shaped by chronic low-grade inflammation and immune dysregulation at systemic, adipose, and placental levels. Pro-inflammatory cytokines, including tumor necrosis factor-α, interleukin-6, and interleukin-1β, disrupt insulin receptor signaling through NF-κB, JAK/STAT–SOCS3, mTOR, and inflammasome-related pathways, thereby amplifying insulin resistance and β-cell stress. Acute-phase proteins such as high-sensitivity C-reactive protein, pentraxin 3, serum amyloid A, and procalcitonin reflect distinct layers of inflammatory activation and may provide complementary value for early risk stratification, although their diagnostic performance is influenced by gestational timing, maternal adiposity, and population heterogeneity. Alterations in leukocyte profiles, neutrophil-to-lymphocyte ratio, monocyte/macrophage activation, Treg dysfunction, Th1/Th17 skewing, oxidative stress, and neutrophil extracellular trap formation further reveal the immune imbalance underlying GDM progression. This review synthesizes current evidence on inflammatory biomarkers and immune mechanisms in GDM, emphasizing their predictive potential, mechanistic relevance, and translational implications for biomarker-guided diagnosis, individualized risk assessment, and future anti-inflammatory interventions.
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BibTeX
@article{zhang2026inflammatory,
title = {{Inflammatory biomarkers and immune dysregulation in gestational diabetes mellitus: emerging mechanisms and therapeutic prospects}},
author = {Qian Zhang and Yang Shu and Yanan Gao},
journal = {Frontiers in Immunology},
year = {2026},
month = oct,
doi = {10.3389/fimmu.2026.1953251},
url = {https://www.frontiersin.org/articles/10.3389/fimmu.2026.1953251},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Inflammatory biomarkers and immune dysregulation in gestational diabetes mellitus: emerging mechanisms and therapeutic prospects
AU - Qian Zhang
AU - Yang Shu
AU - Yanan Gao
PY - 2026
DA - 2026/10/30
JO - Frontiers in Immunology
DO - 10.3389/fimmu.2026.1953251
UR - https://www.frontiersin.org/articles/10.3389/fimmu.2026.1953251
AB - Gestational diabetes mellitus (GDM) is a common pregnancy-related metabolic disorder that increases the risk of adverse maternal and neonatal outcomes and predisposes both mothers and offspring to long-term metabolic disease. Beyond pregnancy-induced insulin resistance, accumulating evidence indicates that GDM is shaped by chronic low-grade inflammation and immune dysregulation at systemic, adipose, and placental levels. Pro-inflammatory cytokines, including tumor necrosis factor-α, interleukin-6, and interleukin-1β, disrupt insulin receptor signaling through NF-κB, JAK/STAT–SOCS3, mTOR, and inflammasome-related pathways, thereby amplifying insulin resistance and β-cell stress. Acute-phase proteins such as high-sensitivity C-reactive protein, pentraxin 3, serum amyloid A, and procalcitonin reflect distinct layers of inflammatory activation and may provide complementary value for early risk stratification, although their diagnostic performance is influenced by gestational timing, maternal adiposity, and population heterogeneity. Alterations in leukocyte profiles, neutrophil-to-lymphocyte ratio, monocyte/macrophage activation, Treg dysfunction, Th1/Th17 skewing, oxidative stress, and neutrophil extracellular trap formation further reveal the immune imbalance underlying GDM progression. This review synthesizes current evidence on inflammatory biomarkers and immune mechanisms in GDM, emphasizing their predictive potential, mechanistic relevance, and translational implications for biomarker-guided diagnosis, individualized risk assessment, and future anti-inflammatory interventions.
SN - 1664-3224
ER -