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Inhibiting certain immune signals halts development of autism in mice

American Association for the Advancement of Science

A new study has identified a subset of immune signaling proteins that are associated with the development of autism. Blocking these proteins during pregnancy in mice eliminated autism-like behavior in offspring, hinting at a potential means to prevent development of the disorder. Increasingly, evidence suggests that alterations in a mother's immune system - particularly in T cells and the immune signaling protein interleukin-17a (IL-17a) - during key periods of fetal neurodevelopment can lead to autism in offspring. Therefore Gloria Choi et al. explored IL-17a in greater detail in mice. Upon mild infection 12 days into pregnancy, mothers experienced immune responses, which led to increased expression of IL-17a in the cortex of the fetus. Analysis by the team revealed that this also led to disorganized neural connections in the cortex of the fetal brain at 18 days into gestation, and, after birth, the offspring demonstrated behaviors associated with autism. However, this did not occur in offspring whose mothers were pretreated with a compound that blocks IL-17a. A transcription factor called RORγt is known to be a critical regulator of the IL-17a pathway, prompting Choi et al. to investigate the offspring of pregnant mothers lacking RORγt. These mothers did not produce IL-17a upon infection, their fetuses did not develop disorganized cortexes, and after birth, their mice offspring demonstrated normal behavior.

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