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Fetal innate immunity contributes to the induction of atypical behaviors in a mouse model of maternal immune activation

bioRxiv, ISSN: 2692-8205
2020
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  • Citations
    1
    • Citation Indexes
      1
      • CrossRef
        1
  • Social Media
    23
    • Shares, Likes & Comments
      23
      • Facebook
        23

Article Description

Maternal immune activation (MIA) increases likelihood of altered neurodevelopmental outcomes. Maternal cytokines are proposed to affect fetal brain development in mice; however, the contribution of fetal immunity to neurodevelopmental disorders is largely unexplored. Here, we show that MIA mediated by Toll-like receptor 3 (TLR3), but not other TLRs, induces a specific set of behavioral phenotypes including decreased sociability and increased restricted repetitive behavior in offspring. Accordingly, these behavioral phenotypes were absent when offspring were deficient for Trif, the downstream adapter molecule of TLR3. Using single-cell RNA sequencing, we identified clusters of border-associated macrophages that were significantly enriched in the fetal brain following TLR3-MIA, and these clusters were diminished in Trif fetal brains. Moreover, we found that triggering TLR3-TRIF in offspring can occur through transplacental viral infection, resulting in altered behavioral phenotypes. Collectively, our data indicate that fetal innate immunity contributes to MIA-induced atypical behaviors in mice.

Bibliographic Details

Eva K. Nichols; Hsiu Chun Chuang; Madeline L. Arnold; Patrick M. Lin; Rhea Misra; Laurent Coscoy; Kaoru Saijo; Matthew T. Davis; Kristina M. Geiger; Rick Z. Li

Cold Spring Harbor Laboratory

Biochemistry, Genetics and Molecular Biology; Agricultural and Biological Sciences; Immunology and Microbiology; Neuroscience; Pharmacology, Toxicology and Pharmaceutics

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