> The reason for that, the researchers found, is that in these mice [with certain genes missing and whose mother didn't have inflammation while pregnant], infla

> The reason for that, the researchers found, is that in these mice [with certain genes missing and whose mother didn't have inflammation while pregnant], inflammation did not stimulate IL-17a production. What I wonder if baseline mice produce IL-17a in response to inflammation? My guess would be no. I would also wonder if some low to moderate infection in mothers can spare the offspring from autism, but still prime IL production?