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The maternal interleukin-17a pathway in mice promotes autism-like phenotypes in offspring
Open accessAbstract
A T cell cause for autism?: The causes of autism spectrum disorder (ASD) are complex and not entirely clear. Alterations in the mother's immune system during pregnancy, especially during key early periods of fetal neurodevelopment, may play a role. Choi et al. provided infectious or inflammatory stimuli to pregnant mice, which resulted in of spring exhibiting behaviors reminiscent of ASD (see the Perspective by Estes and McAllister). A subset of T helper cells that make the cytokine interleukin-17a in the mothers caused cortical defects and associated ASD behaviors in offspring. Therapeutic targeting of interleukin-17a during gestation reduced ASD symptoms in offspring. Science , this issue p. 933 ; see also p. 919
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“MIA can also induce more complex cortical phenotypes such as focal cortical dysplasia [81, 132], similar to those found in ASD [34] (Fig. 7).”
From The ASD Living Biology: from cell proliferation to clinical phenotype (2019) · cites this paper as [132]
In the citing paper
“Also, cytoarchitecture heterogeneity is seen that is characteristic of ASD cases [34, 132].”
From The ASD Living Biology: from cell proliferation to clinical phenotype (2019) · cites this paper as [132]
In the citing paper
“The Choi and colleagues [132, 81] MIA ASD mouse model study showed that the same fetal MIA perturbation of littermates causes patches of focal cortical dysplasia that have marked heterogeneity, analogous to heterogeneity found in cortex in unrelated individual ASD cases postmortem [34] (Fig. 7).”
From The ASD Living Biology: from cell proliferation to clinical phenotype (2019) · cites this paper as [132]
In the citing paper
“treatment of the anti-IL-17 antibody 2 days after MIA induction saw rescue of some phenotypes, such as USV calls and marble burying, but not others, including interaction deficits”
From The Role of the Immune System in Autism Spectrum Disorder (2017) · cites this paper as Choi et al, 2016
In the citing paper
“Given that IL-23 induces IL-17 and the importance of IL-17 for inducing the MIA model of autism (Choi et al, 2016)”
From The Role of the Immune System in Autism Spectrum Disorder (2017) · cites this paper as Choi et al, 2016
In the citing paper
“blocking key pathways prevents MIA-induced neural and behavioral abnormalities in ASD model systems.32”
From Maternal immune activation dysregulation of the fetal brain transcriptome and relevance to the pathophysiology of autism spectrum disorder (2018) · cites this paper as [32]
In the citing paper
“MIA alters proliferation of cortical neural progenitor cells, laminar allocation of neurons, increased cortical thickness, increased cell density and patches of cortical dysplasia.32, 38, 42”
From Maternal immune activation dysregulation of the fetal brain transcriptome and relevance to the pathophysiology of autism spectrum disorder (2018) · cites this paper as [32]
In the citing paper
“Increased systemic IL-17 during pregnancy leads to development of autism-like behaviors in pup offspring (Choi et al., 2016), which can also be regulated by maternal microbiota (Kim et al., 2017).”
From The IL-17 Family of Cytokines in Health and Disease (2019) · cites this paper as Choi et al., 2016
In the citing paper
“The implicated cytokine pathways include, and not limited to, IL-5, IL-15, IL-17, IL-17a, IL-10, IL-1b, TNF-α, TGF-β1 and IFNγ [12, 18, 65, 66].”
From Gut microbiota changes in children with autism spectrum disorder: a systematic review (2020) · cites this paper as [66]
In the citing paper
“Alterations of the host immune responses by gut microbiota are closely linked to ASD-related symptoms.”
From Gut microbiota changes in children with autism spectrum disorder: a systematic review (2020) · cites this paper as [66]
In the citing paper
“A number of biomarkers that could connect to microbial profiles also have been identified in ASD, including alterations in serotonin levels, IL1β, and IL6.35, 44, 45, 46, 47”
From Distinct Microbiome-Neuroimmune Signatures Correlate With Functional Abdominal Pain in Children With Autism Spectrum Disorder (2017) · cites this paper as [35]
In the citing paper
“Abnormal behaviors have also been reported in the absence of microbiota, including decreased anxiety-like behavior in the elevated plus maze21.”
From Meningeal γδ T cells regulate anxiety-like behavior via IL-17a signaling in neurons (2020) · cites this paper as [21]
In the citing paper
“Alleviated anxiety-like behavior has been previously linked to the lack of microbiota21.”
From Meningeal γδ T cells regulate anxiety-like behavior via IL-17a signaling in neurons (2020) · cites this paper as [21]
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Citations
Cites
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“Some studies have reported reduced USV calls upon MIA (8, 31), but these opposite effects may reflect differences in methodological approaches, including dose and number of exposures to poly(I:C) as well as timing of poly(I:C) administration.”
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“To determine if IL-17a acts on receptors in the mother or the fetus to induce the MIA phenotype, we injected poly(I:C) into IL-17Ra WT, HET or KO mothers that had been bred to IL-17Ra WT or HET males (39).”
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“Co nt an tiIL -1 7a PBS Poly(I:C) Co nt an tiIL -1 7a 0 500 1000 1500 2000 To ta l d is ta nc e m ov ed ( cm ) 2500 0 100 200 300 400 U S V in de x Co nt an ti- IL -1 7a PBS Poly(I:C) **** ** Co nt an ti- IL -1 7a 0 20 40 60 80 % In te ra ct io n 100 Social Inanimate ** * ** Co nt an ti- IL -1 7a PBS Poly(I:C) Co nt a…”
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The effect of Chlorella supplementation in pregnant women with low‐grade inflammation
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“For this reason and in order to specifically inactivate ALK in the fetuses without affecting maternal conditions, we adopted an approach (Choi et al. 2016) that directly injected ALK inhibitors ceritinib (Marsilje et al.”
MethodCanales, C. P., Estes, M. L., Cichewicz, K., Angara, K., Aboubechara, J. P., Cameron, S., Prendergast, K., Su-Feher, L., Zdilar, I., Kreun, E. J., et al. (2020) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2020.06.13.150359 · Cited by 3
“Our findings of disrupted cortical lamination following the acute MIA signature are consistent with, but not identical to previous studies showing cortical dysplasia associated with MIAinduced aberrant behavior in offspring (20,34).”
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“Given the importance of maternal Immune activation as a risk factor in neurodevelopmental disorders (Bauman et al, 2014; Estes & McAllister, 2016; Giovanoli et al, 2016; Lipina et al, 2013; Malkova et al, 2012; Missault et al, 2014), our findings that STAT3 and RGS4 expression are upregulated in the brain of embryos e…”
BackgroundMethodInfluentialImmune activation state modulates the retrieval of infant engramsPreprint
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BackgroundChd8 haploinsufficiency leads to molecular layer heterotopias and age-dependent cortical expansionPreprint
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“IL-6 also stimulates the differentiation of th17 cells and downstream release of IL-17A, which is also considered a core driver of MIA-induced pathologies (Choi et al., 2016).”
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BackgroundResultMicrobiota–Gut–Brain Axis in Neurodevelopmental Disorders
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“Cytokines have been shown to play crucial roles in mediating the effects of MIA on offspring [30,31].”
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Key actors in neuropathophysiology: The role of γδ T cells
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“The administration of anti-IL-17 antibodies in pregnant dams ameliorated the symptomatic of MIA-associated behavioural abnormalities [137, 138].”
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“These inflammatory cytokines can affect synaptic plasticity, promote abnormal cortical development, and potentially contribute to the formation of ASD-like phenotypes (Choi et al., 2016; Bhandari et al., 2020).”
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“These de fi cits were preventable by early treatment with anti-IL-17a antibodies or knocking out a speci fi c IL-17 receptor subunit in embryonic neurons [156, 157].”
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Interleukin-17: Why the Worms Squirm
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“Specifically, previous work has demonstrated male-specific alterations to USVs following maternal immune activation (MIA), including decreased call rate and an increase in short calls (Choi et al., 2016; Malkova et al., 2012).”
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“Animal models recapitulate this epidemiological and clinical evidence, as maternal immune activation serves as an established model of ASD in rodents 18–21 and non-immune murine models of ASD also exhibit alterations in neuroinflammation 8,22,23 .”
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Profound Associations between Maternal Infectious Disease and Fetal Neurodevelopmental DelaysPreprint
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IL-17A Alters Human Cortical Development in a 3D Ex Vivo Model of Maternal Immune ActivationPreprint
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Maternal immune activation and neuropsychiatric disease in offspring: Pathogen's perspective
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Emerging Epigenetic Therapeutics and Diagnostics for Autism Spectrum Disorder
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“…be causal, with abnormal neural development and differentiation in mice exposed to cytokines, resulting in changes in their behavioural patterns (Choi et al. 2016; Fujitani et al. 2022; Gumusoglu et al. 2020; Kalish et al. 2021; Loayza et al. 2023; Ozaki et al. 2020; Smith et al. 2007; Wu et…”
Preeclampsia: The silent catalyst for autism spectrum disorder in offspring
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Fetal Neuroassessment and Intrauterine Inflammation: Emerging Perspectives for Term Pregnancies
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Neurogenesis decreases in the offspring of mothers infected with influenza A virus
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Oxytocin Modulates Microglial IL-17-Linked Inflammatory Pathways Through the IL-6/COX-2
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Metadata
- Authors
- Choi, G. B., Yim, Y. S., Wong, H., Kim, S., Kim, H., Kim, S. V., Hoeffer, C. A., Littman, D. R., & Huh, J. R.
- Affiliations
- McGovern Institute for Brain Research (US)
- University of Colorado Boulder (US)
- University of Massachusetts Chan Medical School (US)
- Howard Hughes Medical Institute (US)
- Corresponding author
- Choi, Gloria B.
- Yim, Yeong S.
- Wong, Helen
- Hoeffer, Charles A.
- Littman, Dan R.
- Huh, Jun R.
- ORCID
- Venue
- Science
- Published
- 2016-02-26
- Volume
- 351
- Issue
- 6276
- Pages
- 933-939
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- PMC
- PMC4782964
- OpenAlex
- W2253802357
- Cited by
- 1,214
- References
- 47
- Citations by year
- 2026: 108 · 2025: 137 · 2024: 147 · 2023: 123 · 2022: 155 · 2021: 136 · 2020: 109 · 2019: 82 · 2018: 97 · 2017: 65 · 2016: 50
- FWCI
- 62.36
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- The Journal of the American Medical Association (JAMA) Network (American Medical Association) (submittedVersion)
- DSpace@MIT (Massachusetts Institute of Technology) (submittedVersion, cc-by-nc)
- PMC
- Funders
- Simons Foundation Autism Research Initiative
- Simons Foundation to the Simons Center for the Social Brain at Massachusetts Institute of Technology
- Robert Buxton
- National Research Foundation of Korea (MEST-35B-2011-1-E00012, NRF-2014R1A1A1006089)
- Crohn’s and Colitis Foundation of America (329388)
- Smith Family Foundation
- Searle Scholars Program
- Alzheimer's Association (MNIRGDP-12-258900)
- Brain and Behavior Research Foundation (NARSAD) (21069)
- NIH (F31NS083277, R00DK091508, R01NS086933)
- Howard Hughes Medical Institute
- Topics
- Life Sciences › Neuroscience › Cognitive Neuroscience › Autism Spectrum Disorder Research
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- maternal immune activation, autism spectrum disorder, IL-17A, RORγt, Th17 cells, maternal viral infection, autism-like behavior, fetal brain, prenatal inflammation
- MeSH terms
- Autism Spectrum Disorder, Retinoic Acid Receptor gamma, Animals, Behavior, Animal, Behavioral Symptoms, Cerebral Cortex, Female, Male, Maternal-Fetal Exchange, Mutation, Phenotype, Pregnancy, Prenatal Exposure Delayed Effects, RNA, Messenger, Signal Transduction, Receptors, Retinoic Acid, Antibodies, Blocking, Interleukin-17, Mice, Nuclear Receptor Subfamily 1, Group F, Member 3, Th17 Cells
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