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Abstract
Prenatal infection increases schizophrenia risk, yet mechanisms remain unclear. This dissertation investigates immune activation during pregnancy using poly I:C, a synthetic viral mimic, focusing on IL-6 production. In vitro studies showed poly I:C induced NF-κB activation and IL-6 expression in astrocyte- and macrophage-like cells, while luteolin and C16 inhibited IL-6 but not NF-κB signaling. In vivo, poly I:C elevated IL-6 in pregnant mice, unaffected by luteolin or C16, suggesting pregnancy amplifies inflammatory responses. TLR3 knockout attenuated IL-6 elevation in pregnant mice, identifying TLR3 as a mediator. Findings highlight pregnancy-specific immune modulation and potential therapeutic targets for inflammatory disorders.