This article was published last year, however it is one of my favorites so I have decided to review it here.
The cause for autism is still not known. However, many factors that could effect early brain development have been linked to the disease. Some of these factors include viral infection and elevated levels of IL-17A.
Pregnant mouse dams injected with Poly(I:C), to mimic viral infection, had increased levels of IL-17a in their serum and placenta.
Pups born to pregnant dams given Poly(I:C) had increased expression of IL17Ra in their cortex and exhibited abnormal cortical development in the form of intrusions and protrusions.
Further, pups born to dams administered Poly(I:C) during pregnancy exhibited behavior patterns associated with autism. These phenotypes include early life distress (USV index from an ultrasonic vocalization assay), decreased social interaction (three chamber social approach), and anxiety (marble burying test).
Interestingly, a majority of these phenotypes could be reversed with the administration of anti-IL17a during pregnancy.
This manuscript is unique in that it associates a behavior phenotype with an immunological mechanism. Maternal IL-17a, as the result of viral infection, can cause autism-like phenotypes in offspring.
This brings up a few interesting questions: i) why don’t all mothers with viral infections during pregnancy give birth to children on the autism spectrum? ii) what is the source of the IL-17? (TH17, ILC3, γδ T cells?) iii) Is autism more prevalent among children born to mothers with TH17-related autoimmune or atopic diseases such as asthma, RA, psoriasis, IBD, MS)?