The maternal interleukin-17a pathway in mice promotes autism-like phenotypes in offspring
| Autor: | Gloria B. Choi, Dan R. Littman, Sangdoo Kim, Hyunju Kim, Sangwon V. Kim, Charles A. Hoeffer, Helen Wong, Jun R. Huh, Yeong Shin Yim |
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| Rok vydání: | 2016 |
| Předmět: |
Male
0301 basic medicine Autism Spectrum Disorder Receptors Retinoic Acid Offspring medicine.medical_treatment Retinoic acid Behavioral Symptoms Biology Article Mice 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Immune system Pregnancy RAR-related orphan receptor gamma Blocking antibody medicine Animals RNA Messenger Antibodies Blocking Maternal-Fetal Exchange Cerebral Cortex Multidisciplinary Behavior Animal Effector Interleukin-17 Nuclear Receptor Subfamily 1 Group F Member 3 Phenotype 030104 developmental biology Cytokine chemistry Prenatal Exposure Delayed Effects Mutation Immunology Th17 Cells Female Interleukin 17 030217 neurology & neurosurgery Signal Transduction |
| Zdroj: | Science. 351:933-939 |
| ISSN: | 1095-9203 0036-8075 |
| Popis: | 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 |
| Databáze: | OpenAIRE |
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