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. Author manuscript; available in PMC: 2014 Aug 6.
Published in final edited form as: Ann Neurol. 2013 Aug 6;74(1):11–19. doi: 10.1002/ana.23898

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.

Fig. 6

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.