The maternal interleukin-17a pathway in mice promotes autism-like phenotypes in offspring
Authors
Choi, Gloria B.Yim, Yeong S.
Wong, Helen
Kim, Sangdoo
Kim, Hyunju
Kim, Sangwon V.
Hoeffer, Charles A.
Littman, Dan R.
Huh, Jun R.
UMass Chan Affiliations
UMass Metabolic NetworkProgram in Innate Immunity
Department of Medicine, Division of Infectious Diseases and Immunology
Document Type
Journal ArticlePublication Date
2016-02-26Keywords
Cell BiologyCellular and Molecular Physiology
Immunology and Infectious Disease
Molecular Biology
Metadata
Show full item recordAbstract
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 (RORgammat)-dependent effector T lymphocytes [for example, 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.Source
Science. 2016 Feb 26;351(6276):933-9. Epub 2016 Jan 28. Link to article on publisher's siteDOI
10.1126/science.aad0314Permanent Link to this Item
http://hdl.handle.net/20.500.14038/36685PubMed ID
26822608Related Resources
Link to Article in PubMedae974a485f413a2113503eed53cd6c53
10.1126/science.aad0314