Autism Spectrum disorders (ASD) exhibit a gender bias where boys are affected predominantly. However, the mechanisms underlying resilience in VPA females are not entirely understood. To shed light on this disparity, we utilized an ASD mouse model, the valproic acid (VPA) model where sociability is more affected in males than females. We hypothesized that immunological mechanisms are involved in the resilience of VPA female mice particularly during the juvenile period because this is when they display unique neuroinflammatory patterns. To tackle this hypothesis, we assessed the impact of juvenile exposure to peripheral lipopolysaccharide (LPS)-induced inflammation on adult sociability and neuroinflammation in female mice prenatally exposed to VPA. Our results revealed that females exposed to chronic inflammation after VPA treatment exhibit ASD-related behavioral alterations comparable to males. Surprisingly, we observed that long-lasting neuroinflammatory effect of VPA were reversed when animals were exposed to LPS during the juvenile period. Specifically, VPA females showed an increase in microglia and astrocyte cell density in the cerebellum, and this effect was reversed with LPS treatment. These results revealed the intricate interplay of environmental factors in shaping sociability development, offering insights into potential new treatment strategies.