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Peer-reviewedCC BY 4.0International Journal of Molecular Sciences

Disruption of Placental Immune Privilege by Complications of Pregnancy: Consequences for Maternal and Child Health

  • Wendy Kisaí Mixtega-Ruiz1,2
  • Mariela Contreras Escamilla3
  • Rosalba Sevilla-Montoya4
  • Andrea Olmos-Ortiz2
  • Verónica Zaga-Clavellina5
  • Diana Catalina Castro-Rodríguez2
5 affiliations
  1. 1Doctorado en Ciencias Biológicas, Centro Tlaxcala de Biología de la Conducta, Tlaxcala C.P. 90070, Mexico
  2. 2Departamento de Inmunobioquímica, Instituto Nacional de Perinatología, Isidro Espinosa de los Reyes, Mexico City C.P. 11000, Mexico
  3. 3Departamento de Investigación y Bioterio, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Mexico City C.P. 14080, Mexico
  4. 4Coordinación de Genética y Genómica Humana Instituto Nacional de Perinatología, Mexico City C.P. 11000, Mexico
  5. 5Dirección de Investigación, Instituto Nacional de Perinatología, Isidro Espinosa de los Reyes, Mexico City C.P. 11000, Mexico
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Abstract

Maternal chronic conditions, including obesity, diabetes, hypertensive disorders, and autoimmune diseases, promote a systemic proinflammatory environment characterized by oxidative stress and chronic inflammation. These alterations lead to reduced expressions of human leukocyte antigen-G (HLA-G) and programmed death-ligand 1 (PD-L1), decreased regulatory T (Treg)cell activity, and increased T helper (Th)1/Th17 responses, disrupting placental immune privilege and resulting in increased production of proinflammatory cytokines, oxidative stress, trophoblastic dysfunction, and placental senescence. This change in immune privilege contributes to fetal growth restriction, preterm birth, congenital anomalies, and long-term cardiometabolic programming in offspring. Understanding the mechanisms underlying placental immune dysregulation may facilitate the development of targeted therapeutic strategies aimed at restoring immune tolerance and reducing inflammatory and hypoxic signaling pathways to improve maternal and neonatal outcomes. This review summarizes the current state of the field of placental immunological privilege and how maternal chronic conditions like obesity, diabetes, hypertensive disorders, and autoimmune diseases can disrupt it and its possible consequences on the progeny.

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Cite

BibTeXRIS
BibTeX
@article{mixtegaruiz2026disruption,
  title = {{Disruption of Placental Immune Privilege by Complications of Pregnancy: Consequences for Maternal and Child Health}},
  author = {Wendy Kisaí Mixtega-Ruiz and Mariela Contreras Escamilla and Rosalba Sevilla-Montoya and Andrea Olmos-Ortiz and Verónica Zaga-Clavellina and Diana Catalina Castro-Rodríguez},
  journal = {International Journal of Molecular Sciences},
  year = {2026},
  month = oct,
  doi = {10.3390/ijms27209247},
  url = {https://www.mdpi.com/1422-0067/27/20/9247},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Disruption of Placental Immune Privilege by Complications of Pregnancy: Consequences for Maternal and Child Health
AU  - Wendy Kisaí Mixtega-Ruiz
AU  - Mariela Contreras Escamilla
AU  - Rosalba Sevilla-Montoya
AU  - Andrea Olmos-Ortiz
AU  - Verónica Zaga-Clavellina
AU  - Diana Catalina Castro-Rodríguez
PY  - 2026
DA  - 2026/10/01
JO  - International Journal of Molecular Sciences
DO  - 10.3390/ijms27209247
UR  - https://www.mdpi.com/1422-0067/27/20/9247
AB  - Maternal chronic conditions, including obesity, diabetes, hypertensive disorders, and autoimmune diseases, promote a systemic proinflammatory environment characterized by oxidative stress and chronic inflammation. These alterations lead to reduced expressions of human leukocyte antigen-G (HLA-G) and programmed death-ligand 1 (PD-L1), decreased regulatory T (Treg)cell activity, and increased T helper (Th)1/Th17 responses, disrupting placental immune privilege and resulting in increased production of proinflammatory cytokines, oxidative stress, trophoblastic dysfunction, and placental senescence. This change in immune privilege contributes to fetal growth restriction, preterm birth, congenital anomalies, and long-term cardiometabolic programming in offspring. Understanding the mechanisms underlying placental immune dysregulation may facilitate the development of targeted therapeutic strategies aimed at restoring immune tolerance and reducing inflammatory and hypoxic signaling pathways to improve maternal and neonatal outcomes. This review summarizes the current state of the field of placental immunological privilege and how maternal chronic conditions like obesity, diabetes, hypertensive disorders, and autoimmune diseases can disrupt it and its possible consequences on the progeny.
SN  - 1422-0067
ER  -