Evidence suggests that both genetic and environmental factors are associated with schizophrenia. Maternal infection have been considered a risk factor for schizophrenia. Previous mouse studies showed that maternal immune challenge induced schizophrenia-related abnormal behavior in adults offspring. Postmortem studies have reported the alterations in gene expression and DNA methylation in schizophrenia. Taken together, maternal infection may influence genetic expression and DNA methylation during postnatal brain development, which involve in pathogeneses of schizophrenia. To investigate the transcriptional regulations affected by maternal immune challenge in fetal brain by microarray and ChIP-Seq, which remains throughout development and cause behavioral abnormality in adult. Poly I:C or PBS was administered into pregnant mice every 6 consecutive days from E14 to E19. The offspring were divided into 4 groups: Poly I:C-female, Poly I:C-male, PBS-female and PBS-male-mice. total RNA from prefrontal cortex of adults offspring was applied on Illumina Mouse WG-6 V2 Beadchips to analysis mRNA expression profiling. Methylated DNA was isolated from prefrontal cortex using MethylMiner Methylated DNA Enrichment Kit. Illumina Genome Analyzer IIx was used to analyze DNA methylation profiles. Sequenced reads were mapped to the mouse genome, and target genes-associated peak calls were determined with MACS and GREAT. Poly I:C-male-mice showed decreased %PPI only in 71 dB, whereas Poly I:C-female mice showed significantly decreased %PPI in all of 68, 71 and 77 dB. Specific gene expression profiles and methylation patterns were identified in both of Poly I:C-male and -female mice cam paring with its PBS-control, respectively. Poly I:C-female-mice showed more genes transcript alterations and DNA hypermethylation than male counterparts. Data suggest molecular mechanisms underlying the impact of maternal immune response to the fetal brain, which is preserved until adult and caused behavioral abnormality in gender-specific manner.