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03 vs RUPP). Placental levels of TNF-α, a cNK-secreted cytokine, and MIP-3α, a cNK chemokine, were higher in RUPP vs NP, and lower after IL-17 blockade. Placental VEGF was lower in RUPP vs NP, and was normalized in RUPP+IL-17RC. In vitro cytolytic activity of RUPP placental NKs was higher compared to NP, and was blunted in RUPP+IL-17RC NKs. Finally, both fetal and placental weight were lower in RUPP compared to NP, and were improved in RUPP+IL-17RC. These data identify IL-17 as a mediator of cNK activation in response to placental ischem