Maternal-Fetal Immunobiology

About the Program

The Maternal-Fetal Immunobiology Division investigates immunological pathways that lead to obstetrical disorders, with the goals of improving the understanding of the mechanisms of disease and of developing methods for the early diagnosis, treatment, and prevention of pregnancy complications, with an emphasis on spontaneous preterm labor and birth. We utilize in vivo (wild type, transgenic, and knockout mice) and ex vivo (placental, blood, and amniotic fluid samples) approaches as well as classic and contemporary (e.g. flow cytometry, imaging flow cytometry, fluorescence-activated cell sorting or FACS, confocal microscopy, and multiplex immunohistochemistry) molecular laboratory techniques to understand the molecular and cellular mechanisms responsible for spontaneous preterm labor and birth.


  • To study the mechanisms whereby damage-associated molecular patterns (DAMPs) induce sterile intra-amniotic inflammation and spontaneous preterm labor and birth.
  • To mechanistically elucidate the homeostatic role of innate immune cells in late pregnancy in order to develop novel strategies to prevent inflammation-induced preterm labor and birth.
  • To mechanistically elucidate the roles of effector and regulatory T cells in the pathophysiology of spontaneous preterm labor.
  • To investigate host immune interactions during pregnancy.
  • To study the biology of immune cells in the amniotic cavity and maternal-fetal interface.

Research Highlights

  • Discovered a role for the NRLP3 inflammasome in the mechanisms responsible for normal parturition and spontaneous preterm labor and birth.
  • Generated in vivo evidence suggesting that targeting the NLRP3 inflammasome can be used to treat sterile intra-amniotic inflammation, a clinical condition that currently lacks treatment.
  • Provided a causal link between increased amniotic fluid concentrations of danger signals or alarmins and spontaneous preterm labor/birth.
  • Established animal models of sterile intra-amniotic inflammation by intra-amniotically injecting danger signals of alarmins into the amniotic cavity using high-resolution ultrasound.
  • Provided evidence that Ureaplasma species induce preterm birth and fetal inflammatory injury, which is translated into adverse neonatal outcomes. Such adverse perinatal outcomes are prevented by treatment with clarithromycin.
  • Established a central role for regulatory T cells end effector T cells in the pathophysiology of spontaneous preterm labor and birth and fetal growth restriction.
  • Established a role for fetal CD4+ T cells in the pathophysiology of a subset of idiopathic spontaneous preterm labor cases, which occur in the absence of intra-amniotic inflammation.

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