The autoimmune aspect of preterm labor

A paper just published in PLoS ONE (Public Library of Science) presents findings that expand our understanding of the inflammatory aspect of preterm labor.  The authors state:

"Preterm parturition is characterized by innate immune activation and increased proinflammatory cytokine levels. This well established association leads us to hypothesize that preterm delivery is also associated with neonatal T lymphocyte activation and maturation."

For our lay readership, innate immune activation refers to the cell-mediated 'first phase' Th1 immune response versus the 'second phase' Th2 antibody aspect mediated by T lymphocyte activation. The authors obtained cord blood samples following normal and preterm deliveries, and deliveries complicated by clinical chorioamnionitis (inflammation of the fetal membranes). What did they find?

"Infants born following preterm delivery demonstrated enhanced CD4+ T lymphocyte activation... Neonates delivered following clinical chorioamnionitis also demonstrated increased T cell activation. Preterm neonates had an increased frequency of CD45RO+ T cells."

Autoimmune cross-reactions to environmental stimuli fuels a wide range of disorders. Consider the role of gluten sensitivity in a variety of female reproductive disorders. The authors conclude:

"Preterm parturition is associated with neonatal CD4+ T cell activation, and an increased frequency of CD45RO+ T cells. These findings support the concept that activation of the fetal adaptive immune system in utero is closely associated with preterm labor."

The obvious practical implication is that screening for preterm labor can be accomplished by testing for antibodies to the fetal membranes. In positive cases rational therapy can be applied on a functional basis to address the underlying causes of immune overactivation.