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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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“12,15 Currently, several miRNAs have been implicated in neuropsychiatric disorders.”
BackgroundThe chemokine XCL1 functions as a pregnancy hormone to program offspring innate anxiety
Chen, R. J., Nabila, A., Toth, J. G., Stuhlmann, H., & Tóth, M. (2024) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2024.02.032 · Cited by 3
Neuroinflammation and autism: what have we learned so far?
Aytulun, A., & Ünal, D. (2024) · International Journal of Developmental Disabilities · doi:10.1080/20473869.2024.2366722 · Cited by 5
“Blocking these pathways prevents neural and behavioral anomalies in MIA autism models (Choi et al. 2016).”
He, F., Yu, J., Ma, S., Zhao, W., Zhang, M., Wang, J., Zhang, C., Wu, J., & Zhu, L. (2024) · International Archives of Allergy and Immunology · doi:10.1159/000539703 · Cited by 4
“IL-17 is abundantly expressed in the synovium of RA patients, and the addition of exogenous IL-17 can induce the destruction of collagen, which is also the reason why RA synovial cells are damaged and it is dif fi cult to cure RA patients [14].”
Couch, A. C. M., Brown, A. M., Raimundo, C., Solomon, S., Taylor, M., Sichlinger, L., Matulevičiūtė, R., Srivastava, D. P., & Vernon, A. C. (2024) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2024.08.007 · Cited by 4
Supplier-origin gut microbiomes affect host body weight and select autism-related behaviors
McAdams, Z. L., Gustafson, K. L., Russell, A. L., Self, R., Petry, A. L., Lever, T. E., & Ericsson, A. C. (2024) · Gut Microbes · doi:10.1080/19490976.2024.2385524 · Cited by 4
“13 The application of these distinct supplier-origin communities in the MIA model of ASD provided a unique platform to identify a single bacterial taxon sufficient to induce maternal Th17 responses and ASD-related behavior in the offspring.”
BackgroundCollins, B., Lemanski, E. A., & Wright-Jin, E. C. (2024) · Biomedicines · doi:10.3390/biomedicines12112559 · Cited by 5
Kawiková, I., Hakenova, K., Lebedeva, M., Kletečková, L., Jakob, L., Spicka, V., Wen, L., Španiel, F., & Valeš, K. (2024) · Physiological Research · doi:10.33549/physiolres.935501 · Cited by 5
“Another critical cytokine, IL-17, is required for elicitation of abnormal cortical and altered behavior in offspring, as discovered by Gloria Choi [13].”
Blanchard, A. C., Maximova, A. A., Phillips-Jones, T., Bruce, M. R., Anastasiadis, P., Dionisos, C. V., Engel, K., Reinl, E. L., Pham, A. L., Malaiya, S., et al. (2024) · Developmental Cell · doi:10.1016/j.devcel.2024.11.015 · Cited by 6
Harbi, R. A., & Mouihate, A. (2025) · Neuroscience · doi:10.1016/j.neuroscience.2025.01.055 · Cited by 4
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Tsukada, T., Shimada, H., Sakata‐Haga, H., Shoji, H., Iizuka, H., & Hatta, T. (2021) · Biochemistry and Biophysics Reports · doi:10.1016/j.bbrep.2021.100958 · Cited by 4
“Furthermore, it has been demonstrated that interleukin-17a, as a single or downstream mediator of IL-6, causes abnormal cortical structure and autism spectrum disorder (ASD)-related behavior in offspring exposed to maternal immune activation [13].”
BackgroundNon-immune functions of inflammatory cytokines targeted by anti-psoriatic biologics: a review
Lee, T.-L., & Tsai, T. (2022) · Inflammation Research · doi:10.1007/s00011-021-01528-0 · Cited by 4
“In mouse models, the Th-17 cell/IL-17 pathway was central in the pathogenesis of autism-like behavior in offspring born to dams with inflammatory conditions during gestation [116, 117].”
BackgroundPrendergast, K., & McAllister, A. K. (2022) · Journal of Visualized Experiments · doi:10.3791/64095 · Cited by 4
Data‐driven dissection of the fever effect in autism spectrum disorder
Muller, E., Shalev, I., Bachmat, E., & Eran, A. (2023) · Autism Research · doi:10.1002/aur.2935 · Cited by 4
“It should be noted that the accumulating knowledge of the fever effect remains limited as most studies were conducted on animal models of ASD (Choi et al., 2016; Reed et al., 2020), relied on modest sample sizes, and, when applied to humans were based on parental reports and/or retrospective memory…”
BackgroundDu, J., Nakachi, Y., Murata, Y., Kiyota, E., Kato, T., Bundo, M., & Iwamoto, K. (2024) · Psychiatry and Clinical Neurosciences · doi:10.1111/pcn.13640 · Cited by 4
Neuromodulation: The Fevered Mind of the Worm
Ringstad, N. (2017) · Current Biology · doi:10.1016/j.cub.2017.03.005 · Cited by 4
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“(3) The gross monthly influenza incidences were adjusted base”
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Application of brain organoids in neurodevelopmental disorders
Zhao, C., Qi, Y., Xia, L., Zhu, T., & Xia, K. (2025) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2025.152405 · Cited by 3
Nabila, A., Sciortino, R. K., Politowska, N., Brindley, E., Hámor, P. U., Zallar, L. J., Toth, J. G., Pleil, K. E., & Tóth, M. (2025) · Cell Reports · doi:10.1016/j.celrep.2025.116219 · Cited by 3
Dong, B., Chang, M., Liu, J., Li, K., Xiao, H., Wu, S., Feng, D., & Guo, B. (2025) · Molecular Psychiatry · doi:10.1038/s41380-025-03349-7 · Cited by 3
“Choi et al. [54] further demonstrated that IL-17A is produced by maternal Th17 cells.”
InfluentialKubo, A., Kamiya, S., Sanaka, S., Nakamura, K., Kishi, K., & Sasaki, T. (2025) · Neuroglia · doi:10.3390/neuroglia6040045 · Cited by 4
“In parallel, microglia were shown to be indispensable for MIA-induced fetal brain responses [9].”
InfluentialPrenatal electroacupuncture modulates maternal-fetal immune activation via a brain-to-splenic signal
Zhang, Z.-Q., Lin, W.-P., Yan, J.-L., Wang, X., Wang, J., Wang, F., He, T., Xu, J., Xia, Y., & Chen, Y. (2025) · Cell Reports · doi:10.1016/j.celrep.2025.116576 · Cited by 3
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“Preclinical studies show male-speci fi c alterations in cortical architecture and synaptic organization after MIA exposure [13, 14, 62, 63].”
InfluentialThe Ketogenic Diet: An Anti-Inflammatory Treatment for Schizophrenia?
Hung, A., Krycer, J. R., Sarnyai, Z., Palmer, C., & Navarro, S. (2025) · Journal of Inflammation Research · doi:10.2147/jir.s540859 · Cited by 3
“41 Specifically, preclinical evidence indicates that IL-17A impairs the migration and maturation of cortical inhibitory interneurons, particularly parvalbumin-positive (PV) gamma-aminobutyric acid (GABA)ergic inhibitory interneurons, which are essential for coordinated cortical activity and…”
Microbiota regulation of gut-brain neuroimmune crosstalk in early life
Ravisankar, P., Wong, D. S. H., & Zeng, M. Y. (2025) · International Immunology · doi:10.1093/intimm/dxaf076 · Cited by 4
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Oral tolerance to systemic vaccination remains intact without RORγt expression in regulatory T cells
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Maternal immunoglobulin G affects brain development of mouse offspring
Sadakata, M., Fujii, K., Kaneko, R., Hosoya, E., Sugimoto, H., Kawabata‐Iwakawa, R., Kasamatsu, T., Hongo, S., Koshidaka, Y., Takase, A., et al. (2024) · Journal of Neuroinflammation · doi:10.1186/s12974-024-03100-z · Cited by 4
“Analyses of maternal immune activation (MIA) mouse models have shown that maternal interleukin (IL)-17a promotes autistic behavior in pups [67].”
BackgroundNeuro-immune interactions in memory
Stewart, E., & Ryan, T. J. (2025) · Neurobiology of Learning and Memory · doi:10.1016/j.nlm.2025.108077 · Cited by 3
“Injection of Poly(I:C) at embryonic day 12.5 results in increases in inflammatory cytokines such as IL-6 and IL-17A that drive an inflammatory cascade within the foetal compartment resulting in neurodevelopmental perturbations (Smith et al. , 2007; Choi, 2016).”
InfluentialA mother's touch: microbial guardians of early immune imprinting
Zeng, M. Y., & Brown, J. A. (2025) · Trends in Immunology · doi:10.1016/j.it.2025.09.008 · Cited by 3
Features of the cytokine profile in children with autism spectrum disorder
Khudiakova, M. I., Черевко, Н. А., Новиков, П. С., & Berezovskaia, K. V. (2021) · Bulletin of Siberian Medicine · doi:10.20538/1682-0363-2020-4-174-178 · Cited by 4
Peptoniphilus indolicus infection in a pregnant woman: a case report
Ji, C., Xu, F., Wang, Y., & Qin, Y. (2022) · Current Medical Research and Opinion · doi:10.1080/03007995.2022.2072091 · Cited by 3
Pronostiquer tôt les troubles du spectre autistique : Un défi ?
Ben‐Ari, Y., Caly, H., Rabiei, H., & Lemonnier, É. (2022) · médecine/sciences · doi:10.1051/medsci/2022054 · Cited by 3
Lacorcia, M., Kugyelka, R., Spechtenhauser, L., Prodjinotho, U. F., Hamway, Y., Spangenberg, T., & da Costa, C. P. (2022) · Frontiers in Immunology · doi:10.3389/fimmu.2022.878029 · Cited by 3
“Maternal viral infection during pregnancy has been linked to numerous developmental changes, and has become explored experimentally through maternal immune activation models (26) .”
BackgroundInfluentialApplication of machine learning in early identification and diagnosis of autistic children
Tingting, H. O. U., Xiao, C. H. E. N., Kong, D., Xiujun, S. H. A. O., Lin, F., & Kaiyun, L. I. (2022) · Advances in Psychological Science · doi:10.3724/sp.j.1042.2022.02321 · Cited by 3
Lee, K. H., Kiupel, M., Woods, T., Pingle, P., & Hardy, J. W. (2022) · Pediatric Research · doi:10.1038/s41390-022-02307-1 · Cited by 4
“Injection of the bacterial endotoxin lipopolysaccharide (LPS) or polyinosinic-polycytidylic acid [poly(I:C)], which mimics viral infections, activates the immune system of pregnant rodents and results in altered brain gene expression(4) and atypical behavior in offspring.(5) These behavioral abnormalities are notably…”
BackgroundPrenatal programming of the brain: The maternal-fetal interface takes center stage
Antonson, A. M. (2023) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2023.01.019 · Cited by 3
Potential approaches and recent advances in biomarker discovery in autism spectrum disorders
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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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