Since increased levels of TNF-α have previously been described in GDM placentae or patient sera (49, 51, 52), we examined this aspect in our study. Our data confirm that circulatory TNF-α levels are elevated in our study cohort when compared to the control group. The priming activity of TNF-α on neutrophils is well described (47). To confirm that TNF-α contributes to neutrophil priming in GDM, we used infliximab, a clinically employed antagonist. The addition of this agent to isolated neutrophils treated with GDM plasma significantly diminished the occurrence of NETs in in vitro cultures. These findings, hence, suggest that circulatory TNF-α plays a key role in mediating neutrophil activation in cases with GDM.