GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE230nnn/GSE230252/primaryOK200TranscriptomicsRattus norvegicusExpression profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE230252GEOGSEfalseThe imbalance of Th17/Treg cells induced by prenatal chronic stress exposure is associated with activation of the PI3K/Akt/NF-κB signaling pathway in offspringMaternal immune dysregulation, caused by gestational psychological stress, infection, and other perturbations, results in altered offspring immune development and increases risk for immune related disorders. However, the number of studies reporting the effects of prenatal stress on immune system of offspring is very limited. In this study, we examined whether prenatal stress stimuli, based on the CUMS model, may activate the PI3K/Akt/NF-κB signaling pathway and cause an imbalance of Treg/Th17 in the offspring's spleen. Through the establishment of CUMS model, we discovered that prenatal stress increased the plasma levels of corticosterone, IL-1β and IL-6 in the rats that were exposed to it, as well as the serum levels of IL-6, TNF-α and TGF-β in the offspring. We also discovered a correlation between the levels of cytokines in the female rats and the offspring. Additionally, the outcomes of the transcriptome sequencing and PCR experiment demonstrated that the differentially expressed mRNAs in offspring exposed to prenatal stress may cause an imbalance of Th17/Treg via activating the Gng3-related PI3K/Akt/NF-B pathway.2026/04/21GSE230252GSM7210820GSM7210813GSM7210812GSM7210811GSM7210810GSM7210817GSM7210806GSM7210816GSM7210805GSM7210815GSM7210814GSM7210809GSM7210819GSM7210808GSM7210807GSM721081818694230252Rattus norvegicus