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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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In the citing paper
“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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Self-citationFunctional Specialization of Interleukin-17 Family Members
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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…”
BackgroundInfluentialPeñagarikano, O., Abrahams, B. S., Herman, E. I., Winden, K. D., Gdalyahu, A., Dong, H., Sonnenblick, L. I., Gruver, R., Almajano, J., Bragin, A., et al. (2011) · Cell · doi:10.1016/j.cell.2011.08.040 · Cited by 1,075 · cited 1×
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BackgroundImmune involvement in schizophrenia and autism: Etiology, pathology and animal models
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Requirement for RORγ in Thymocyte Survival and Lymphoid Organ Development
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BackgroundSelf-citationPatches of Disorganization in the Neocortex of Children with Autism
Stoner, R., Chow, M. L., Boyle, M. P., Sunkin, S. M., Mouton, P. R., Roy, S., Wynshaw-Boris, A., Colamarino, S. A., Lein, E. S., & Courchesne, E. (2014) · New England Journal of Medicine · doi:10.1056/nejmoa1307491 · Cited by 722 · cited 1×
“1, H and I); (ii) Cortical development starts approximately at E11 (20), which aligns well with the time points of potential fetal exposure to MIA (7); (iii) Disorganized cortex and focal patches of abnormal laminar cytoarchitecture have been found in the brains of ASD patients (21, 22); and (iv) MIA has been shown to…”
BackgroundMalkova, N. V., Yu, C. Z., Hsiao, E. Y., Moore, M. J., & Patterson, P. H. (2012) · Brain, Behavior, and Immunity · doi:10.1016/j.bbi.2012.01.011 · Cited by 662 · cited 3×
“As previously reported (7, 8), we found that prenatal exposure to MIA also caused social interaction deficits in adult offspring (Fig.”
BackgroundSatb2 Regulates Callosal Projection Neuron Identity in the Developing Cerebral Cortex
Alcamo, E. A., Chirivella, L., Dautzenberg, M., Dobreva, G., Fariñas, I., Grosschedl, R., & McConnell, S. K. (2008) · Neuron · doi:10.1016/j.neuron.2007.12.012 · Cited by 658 · cited 15×
“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…”
InfluentialCell-cycle control and cortical development
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BackgroundIn vivo equilibrium of proinflammatory IL-17+ and regulatory IL-10+ Foxp3+ RORγt+ T cells
Lochner, M., Peduto, L., Cherrier, M., Sawa, S., Vives, F. L., Varona, R., Riethmacher, D., Si‐Tahar, M., Santo, J. P. D., & Eberl, G. (2008) · The Journal of Experimental Medicine · doi:10.1084/jem.20080034 · Cited by 557 · cited 3×
“In these animals, the functions of TH17 cells (CD4RORγt cells) and other RORγt-expressing αβT cells are inhibited, but there is no effect in RORγtexpressing innate (or innate-like) immune cells, including γδT, lymphoid tissue-inducer (LTi) cells, and innate lymphoid cells type 3 (ILC3) (11, 12), as well as in RORγexpr…”
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Digoxin and its derivatives suppress TH17 cell differentiation by antagonizing RORγt activity
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Self-citationThe immune response in autism: a new frontier for autism research
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Thymic Origin of Intestinal αß T Cells Revealed by Fate Mapping of RORγt + Cells
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Self-citationAssociation of Family History of Autoimmune Diseases and Autism Spectrum Disorders
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Activation of the maternal immune system induces endocrine changes in the placenta via IL-6
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“Of note, in agreement with previous reports (7, 40), IL-6 injection into pregnant WT mothers was sufficient to produce MIAassociated behavioral (enhanced USV) and cortical phenotypes in the offspring (fig.”
ResultElevated maternal C-reactive protein and autism in a national birth cohort
Brown, A. S., Sourander, A., Hinkka-Yli-Salomäki, S., McKeague, I. W., Sundvall, J., & Surcel, H.-M. (2014) · Molecular Psychiatry · doi:10.1038/mp.2012.197 · Cited by 343
Modeling an autism risk factor in mice leads to permanent immune dysregulation
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“Similarly, in the MIA mouse model, CD4+ T lymphocytes from affected offspring produced higher levels of IL-17a upon in vitro activation (17, 18).”
BackgroundMaternal hospitalization with infection during pregnancy and risk of autism spectrum disorders
Lee, B. K., Magnusson, C., Gardner, R. M., Blomström, Å., Newschaffer, C. J., Burstyn, I., Karlsson, H., & Dalman, C. (2015) · Brain, Behavior, and Immunity · doi:10.1016/j.bbi.2014.09.001 · Cited by 337
Plasma Cytokine Profiles in Subjects with High-Functioning Autism Spectrum Disorders
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“For example, elevated levels of IL-17a, the predominant TH17 cytokine, have been detected in the serum of a subset of autistic children (14, 15).”
BackgroundHoeffer, C. A., Tang, W., Wong, H., Santillan, A., Patterson, R. J., Martinez, L. A., Tejada-Simon, M. V., Paylor, R. E., Hamilton, S. L., & Klann, E. (2008) · Neuron · doi:10.1016/j.neuron.2008.09.037 · Cited by 240 · cited 1×
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MethodSelf-citationDeciphering the role of Th17 cells in human disease
Wilke, C. M., Bishop, K., Fox, D. A., & Zou, W. (2011) · Trends in Immunology · doi:10.1016/j.it.2011.08.003 · Cited by 232
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“3A), in agreement with previous studies (29, 30).”
MethodResultElevated serum levels of interleukin-17A in children with autism
AL-Ayadhi, L. Y., & Mostafa, G. A. (2012) · Journal of Neuroinflammation · doi:10.1186/1742-2094-9-158 · Cited by 196 · cited 1×
“For example, elevated levels of IL-17a, the predominant TH17 cytokine, have been detected in the serum of a subset of autistic children (14, 15).”
BackgroundTh17 Cells Mediate Clade-Specific, Serotype-Independent Mucosal Immunity
Chen, K., McAleer, J. P., Lin, Y., Paterson, D. L., Zheng, M., Alcorn, J. F., Weaver, C. T., & Kolls, J. K. (2011) · Immunity · doi:10.1016/j.immuni.2011.10.018 · Cited by 186
CTIP1 and CTIP2 are differentially expressed during mouse embryogenesis
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“5, as well as in the adult brain, using antibodies specific for proteins expressed in the cortex in a layer-specific manner (25): special AT-rich sequence-binding protein 2 (SATB2) (26), T-brain-1 (TBR1) (27), and chicken ovalbumin upstream promoter transcription factor–interacting protein 2 (CTIP2) (28).”
BackgroundFocal cortical dysplasias in autism spectrum disorders
Casanova, M. F., El-Baz, A. S., Kamat, S. S., Dombroski, B. A., Khalifa, F., Elnakib, A., Soliman, A., Allison-McNutt, A., & Switala, A. E. (2013) · Acta Neuropathologica Communications · doi:10.1186/2051-5960-1-67 · Cited by 150 · cited 1×
“1, H and I); (ii) Cortical development starts approximately at E11 (20), which aligns well with the time points of potential fetal exposure to MIA (7); (iii) Disorganized cortex and focal patches of abnormal laminar cytoarchitecture have been found in the brains of ASD patients (21, 22); and (iv) MIA has been shown to…”
BackgroundGene-Network Analysis Identifies Susceptibility Genes Related to Glycobiology in Autism
van der Zwaag, B., Franke, L., Poot, M., Hochstenbach, R., Spierenburg, H. A., Vorstman, J. A. S., van Daalen, E., de Jonge, M. V., Verbeek, N. E., Brilstra, E. H., et al. (2009) · PLoS ONE · doi:10.1371/journal.pone.0005324 · Cited by 147
SHORT COMMUNICATION: Circulating and Decidual Th17 Cell Levels in Healthy Pregnancy
Nakashima, A., Ito, M., Yoneda, S., Shiozaki, A., 日高, 隆., & Saito, S. (2009) · American Journal of Reproductive Immunology · doi:10.1111/j.1600-0897.2009.00771.x · Cited by 141
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“1, H and I); (ii) Cortical development starts approximately at E11 (20), which aligns well with the time points of potential fetal exposure to MIA (7); (iii) Disorganized cortex and focal patches of abnormal laminar cytoarchitecture have been found in the brains of ASD patients (21, 22); and (iv) MIA has been shown to…”
BackgroundOrosco, L. A., Ross, A. P., Cates, S. L., Scott, S. E., Wu, D., Sohn, J., Pleasure, D., Pleasure, S. J., Adamopoulos, I. E., & Zarbalis, K. S. (2014) · Nature Communications · doi:10.1038/ncomms5692 · Cited by 90
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“3A), in agreement with previous studies (29, 30).”
ResultIL-17 Increased in the Third Trimester in Healthy Women with Term Labor
Martínez-García, E. A., Chávez-Robles, B., Sánchez‐Hernández, P. E., Núñez-Atahualpa, L., Martín-Márquez, B. T., Muñoz-Gómez, A., González-López, L., Gámez-Nava, J. I., Salazar-Páramo, M., Dávalos‐Rodríguez, I. P., et al. (2010) · American Journal of Reproductive Immunology · doi:10.1111/j.1600-0897.2010.00893.x · Cited by 63
Emerging new roles of Th17 cells
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Preferential development of Th17 cells in offspring of immunostimulated pregnant mice
Mandal, M., Marzouk, A. C., DONNELLY, R. J., & Ponzio, N. M. (2010) · Journal of Reproductive Immunology · doi:10.1016/j.jri.2010.06.156 · Cited by 38 · cited 1×
“Similarly, in the MIA mouse model, CD4+ T lymphocytes from affected offspring produced higher levels of IL-17a upon in vitro activation (17, 18).”
BackgroundMaternal Immune Activation Increases Neonatal Mouse Cortex Thickness and Cell Density
Smith, S. E. P., Elliott, R. M., & Anderson, M. P. (2012) · Journal of Neuroimmune Pharmacology · doi:10.1007/s11481-012-9372-1 · Cited by 34 · cited 1×
“1, H and I); (ii) Cortical development starts approximately at E11 (20), which aligns well with the time points of potential fetal exposure to MIA (7); (iii) Disorganized cortex and focal patches of abnormal laminar cytoarchitecture have been found in the brains of ASD patients (21, 22); and (iv) MIA has been shown to…”
BackgroundHoeffer, C. A., Wong, H., Cain, P., Levenga, J., Cowansage, K. K., Choi, Y. Y., Davy, C., Majmundar, N. J., McMillan, D. R., Rothermel, B. A., et al. (2013) · Journal of Neuroscience · doi:10.1523/jneurosci.3513-12.2013 · Cited by 17
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“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.”
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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
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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