HealthDay News — Fetal inflammation and rejection of maternal antigens is associated with uterine contractility and aberrant fetal immune responses, which may play a role in preterm labor (PTL), according to a study published in the April 25 issue of Science Translational Medicine.
Noting that PTL may represent a breakdown in maternal-fetal tolerance, Michela Frascoli, PhD, from the University of California in San Francisco, and colleagues analyzed maternal and cord blood in patients with PTL and in healthy term controls.
The researchers found that cord blood from preterm infants had higher amounts of inflammatory cytokines and greater dendritic cell activation. Preterm cord blood was characterized by a population of central memory cells with a type 1 T helper phenotype, which was not seen in term infants, and by an increase in maternal microchimerism. Compared with term infants, T cells from preterm infants mounted a robust proliferative, proinflammatory response to maternal antigens, but did not respond to third-party antigens. T cells from preterm infants stimulated contractility of the uterine myometrium through interferon-γ and tumor necrosis factor-α. In mouse fetuses, adoptive transfer of activated T cells resulted in pregnancy loss.
“Our findings indicate that fetal inflammation and rejection of maternal antigens can contribute to the signaling cascade that promotes uterine contractility and that aberrant fetal immune responses should be considered in the pathogenesis of PTL,” the authors write.
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