Sequential perturbations to mouse corticogenesis following in utero maternal immune activation

Canales, Cesar P; Estes, Myka L.; Cichewicz, Karol; Angara, Kartik; Aboubechara, John Paul; Cameron, Scott A.; Prendergast, Kathryn; Su-Feher, Linda; Zdilar, Iva; Kreun, Ellie J; Connolly, Emma C; Seo, Jin Myeong; Goon, Jack B; Farrelly, Kathleen; Stradleigh, Tyler W.; List, Deborah van der; Haapanen, Lori; Water, Judy Van de; Vogt, Daniel; McAllister, A. Kimberley; Nord, A.

doi:10.7554/elife.60100

Cited by 23 publications

(32 citation statements)

References 88 publications

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“…Interestingly, Choi et al found that poly (I:C)-induced MIA and IL-17A administration to the embryonic brain on E14.5 resulted in patch-like cortical dysplasia on E18.5 (25), which is similar to some human patients with ASD (30). Their group reproduced the results by another study (31); however, another group mentioned that they could not find any patches after MIA; therefore, the occurrence of cortical patches remains controversial (32).…”

Section: Relationship Between Il-17 Exposure and Asd In The Rodent Em...mentioning

confidence: 86%

Maternal and Adult Interleukin-17A Exposure and Autism Spectrum Disorder

et al. 2022

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Epidemiological evidence in humans has suggested that maternal infections and maternal autoimmune diseases are involved in the pathogenesis of autism spectrum disorder. Animal studies supporting human results have shown that maternal immune activation causes brain and behavioral alterations in offspring. Several underlying mechanisms, including interleukin-17A imbalance, have been identified. Apart from the pro-inflammatory effects of interleukin-17A, there is also evidence to support the idea that it activates neuronal function and defines cognitive behavior. In this review, we examined the signaling pathways in both immunological and neurological contexts that may contribute to the improvement of autism spectrum disorder symptoms associated with maternal blocking of interleukin-17A and adult exposure to interleukin-17A. We first describe the epidemiology of maternal immune activation then focus on molecular signaling of the interleukin-17 family regarding its physiological and pathological roles in the embryonic and adult brain. In the future, it may be possible to use interleukin-17 antibodies to prevent autism spectrum disorder.

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Section: Relationship Between Il-17 Exposure and Asd In The Rodent Em...mentioning

confidence: 86%

Maternal and Adult Interleukin-17A Exposure and Autism Spectrum Disorder

et al. 2022

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“…In another ASD model of maternal immune activation (MIA), we found that klf7 was upregulated at E17.5 and downregulated at P0 [ 55 ]. Epidemiological evidence is growing that environmental exposure early in development has an impact on ASD susceptibility later in life [ 56 ].…”

Section: Discussionmentioning

confidence: 99%

Krüppel-like Transcription Factor 7 Is a Causal Gene in Autism Development

Qiao

Zhao

Jin

et al. 2022

IJMS

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Background: Autism spectrum disorder (ASD) is a complex neurodevelopmental disease. To date, more than 1000 genes have been shown to be associated with ASD, and only a few of these genes account for more than 1% of autism cases. Klf7 is an important transcription factor of cell proliferation and differentiation in the nervous system, but whether klf7 is involved in autism is unclear. Methods: We first performed ChIP-seq analysis of klf7 in N2A cells, then performed behavioral tests and RNA-seq in klf7+/− mice, and finally restored mice with adeno-associated virus (AAV)-mediated overexpression of klf7 in klf7+/− mice. Results: Klf7 targeted genes are enriched with ASD genes, and 631 ASD risk genes are also differentially expressed in klf7+/− mice which exhibited the core symptoms of ASD. When klf7 levels were increased in the central nervous system (CNS) in klf7+/− adult mice, deficits in social interaction, repetitive behavior and majority of dysregulated ASD genes were rescued in the adults, suggesting transcriptional regulation. Moreover, knockdown of klf7 in human brain organoids caused dysregulation of 517 ASD risk genes, 344 of which were shared with klf7+/− mice, including some high-confidence ASD genes. Conclusions: Our findings highlight a klf7 regulation of ASD genes and provide new insights into the pathogenesis of ASD and promising targets for further research on mechanisms and treatments.

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“…OPEN ACCESS radial migration, and cell type composition in the cortex. These alterations have long-lasting effects on brain functional maturation and animal behavior [29,59,60]. Cortical GABAergic neurons reportedly exhibit specific vulnerability to environmental insults [59,61].…”

Section: Trends In Neurosciencesmentioning

confidence: 99%