When a mother experiences an infection during pregnancy and her immune system produces elevated levels of the molecule Interleukin-17a (IL-17a), that can not only alter brain development in her fetus, but also alter her microbiome such that after birth the newborn’s immune system can become primed for future inflammatory attacks.
Using a multi-pronged approach including immunology, germ-free models, neuroscience, and behavioral assays, a team led by scientists at Harvard Medical School and the Massachusetts Institute of Technology investigated the mechanistic underpinnings of immune dysfunction in animal models of autism. The study showed changes in the gut microbiota of pregnant mice following immune activation affect chromatin accessibility in a subset of T cells in their offspring, priming them for immune activation and inflammatory attacks of the gut after birth.
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