The maternal interleukin-17a pathway in mice promotes autism-like phenotypes in offspring
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Choi_The maternal interleukin.pdf
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Author(s)
Choi, Gloria
Yim, Yeong Shin
Wong, Helen
Kim, Sangdoo
Kim, Hyunju
Kim, Sangwon V.
Hoeffer, Charles A.
Littman, Dan R.
Huh, Jun R.
Date Issued
January 2016
Journal
Science
Publisher
American Association for the Advancement of Science (AAAS)
Citation
Choi, G. B., Y. S. Yim, H. Wong, S. Kim, H. Kim, S. V. Kim, C. A. Hoeffer, D. R. Littman, and J. R. Huh. “The Maternal Interleukin-17a Pathway in Mice Promotes Autism-Like Phenotypes in Offspring.” Science 351, no. 6276 (January 28, 2016): 933–939.
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Author's final manuscript
Abstract
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 gamma t (RORγt)–dependent effector T lymphocytes [for example, T helper 17 (T[subscript H]17) 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 T[subscript H]17 cells in susceptible pregnant mothers may reduce the likelihood of bearing children with inflammation-induced ASD-like phenotypes.
MIT Department
Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences
McGovern Institute for Brain Research at MIT
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Article is made available in accordance with the publisher's policy and may be subject to US copyright law. Please refer to the publisher's site for terms of use.
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DOI of Published Version
https://doi.org/10.1126/science.aad0314
