Maternal immune activation (MIA) during pregnancy has been increasingly recognized as a critical factor in the development of neurodevelopmental disorders, with potential sex-specific impacts that are not yet fully understood. In this study, we utilized a murine model to explore the behavioral and molecular consequences of MIA induced by lipopolysaccharide (LPS) administration on embryonic day 12.5. Our findings indicate that male offspring exposed to LPS exhibited significant increases in anxiety-like and depression-like behaviors, while female offspring did not show comparable changes. Molecular analyses revealed alterations in pro-inflammatory cytokine levels and synaptic gene expression in male offspring, suggesting that these molecular disruptions may underlie the observed behavioral differences. These results emphasize the importance of considering sex as a biological variable in studies of neurodevelopmental disorders and highlight the need for further molecular investigations to understand the mechanisms driving these sex-specific outcomes. Our study contributes to the growing evidence that prenatal immune challenges play a pivotal role in the etiology of neurodevelopmental disorders and underscores the potential for sex-specific preventative approaches of MIA.

Myeloid-derived suppressor cells (MDSCs) are heterogeneous cell populations that promote tumor development by inhibiting innate and adaptive immunity. Under physiological conditions, neutrophils have a short survival time in vivo. However, G-MDSCs accumulate abnormally in most tumor hosts, and the mechanisms underlying G-MDSC persistence remain to be clarified. This study utilized flow cytometric analysis and in vivo assays to elucidate these mechanisms. It was observed that the apoptosis of G-MDSCs in the peripheral blood of mice was reduced under tumor conditions, whereas an increase in granulocyte colony-stimulating factor (G-CSF) promoted the survival of G-MDSCs. Furthermore, G-CSF reduced the apoptosis of G-MDSCs by activating the Erk/CREB pathway. Thus, inhibition of G-CSF/Erk/CREB signaling may promote the apoptosis of G-MDSCs and shorten their persistence under tumor conditions, as well as attenuate tumor progression.