alexa The maternal interleukin-17a pathway in mice promotes autismlike phenotypes in offspring
Reproductive Medicine

Reproductive Medicine

Clinics in Mother and Child Health

Author(s): Gloria B Choi, Yeong S Yim, Helen Wong, Sangdoo Kim, Hyunju Kim

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Viral infection during pregnancy has been correlated with increased frequency of autism spectrum disorder (ASD) in offspring. This observation has been modeled in rodents subjected to maternal immune activation (MIA). The immune cell populations critical in the MIA model have not been identified. Using both genetic mutants and blocking antibodies in mice, we show that retinoic acid receptor–related orphan nuclear receptor γt (RORγt)–dependent effector T lymphocytes [e.g., T helper 17 (TH17) cells] and the effector cytokine interleukin-17a (IL-17a) are required in mothers for MIA-induced behavioral abnormalities in offspring. We find that MIA induces an abnormal cortical phenotype, which is also dependent on maternal IL-17a, in the fetal brain. Our data suggest that therapeutic targeting of TH17 cells in susceptible pregnant mothers may reduce the likelihood of bearing children with inflammation-induced ASD-like phenotypes

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This article was published in Science and referenced in Clinics in Mother and Child Health

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