Fig. 6. The proposed involvement of IL-6 and IL-1β as components of maternal immune activation (MIA) in the development of epilepsy and autism-like impairments in the offspring.
Among various components of the MIA triggered by infection (mimicked by PIC in the present studies), IL-6 is necessary and sufficient for producing autism in the offspring in the adulthood. At the same time, the combined induction of IL-6 and IL-1β is both sufficient and necessary for increasing propensity to epilepsy in the offspring. The exposure to a second hit (mimicked by the kindling procedure in these studies) then may produce full epileptic phenotype. Hence, according to the proposed model, the autism-epilepsy comorbidity following an infection during pregnancy depends on the extent of the exposure of fetal brain to IL-6 and IL-1β.