Abstract
Intra-amniotic infection and/or pro-inflammatory cytokine production reduces the rate of respiratory distress syndrome (RDS) in preterm neonates. We previously demonstrated that the first born neonate of multifetal pregnancies was most susceptible to pro-inflammatory immune activation. Cytokine binding to its receptor initiates pro-inflammatory activity. TNFR2 is the receptor for tumor necrosis factor-α on immune and endothelial cells. We examined whether a T>G polymorphism in the TNFR2 gene influenced the rate of RDS in multifetal pregnancies.
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