• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

自闭症谱系障碍啮齿动物模型中异常的白细胞介素-17 水平:系统评价。

Aberrant IL-17 Levels in Rodent Models of Autism Spectrum Disorder: A Systematic Review.

机构信息

School of Pharmacy and Biomedical Sciences, University of Central Lancashire, Preston, United Kingdom.

Laboratory on Thymus Research, Oswaldo Cruz Foundation, Oswaldo Cruz Institute, Rio de Janeiro, Brazil.

出版信息

Front Immunol. 2022 Jun 10;13:874064. doi: 10.3389/fimmu.2022.874064. eCollection 2022.

DOI:10.3389/fimmu.2022.874064
PMID:35757754
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9226456/
Abstract

UNLABELLED

Autism spectrum disorder (ASD) is a heterogeneous neurodevelopmental disorder characterised by stereotyped behaviours, specific interests, and impaired communication skills. Elevated levels of pro-inflammatory cytokines, such as interleukin-17A (IL-17A or IL-17), have been implicated as part of immune alterations that may contribute to this outcome. In this context, rodent models have helped elucidate the role of T-cell activation and IL-17 secretion in the pathogenesis of ASD. Regarding the preclinical findings, the data available is contradictory in offspring but not in the pregnant dams, pointing to IL-17 as one of the main drivers of altered behaviour in some models ASD, whilst there are no alterations described in IL-17 levels in others. To address this gap in the literature, a systematic review of altered IL-17 levels in rodent models of ASD was conducted. In total, 28 studies that explored IL-17 levels were included and observed that this cytokine was generally increased among the different models of ASD. The data compiled in this review can help the choice of animal models to study the role of cytokines in the development of ASD, seeking a parallel with immune alterations observed in individuals with this condition.

SYSTEMATIC REVIEW REGISTRATION

PROSPERO, identifier CRD42022306558.

摘要

未加标签

自闭症谱系障碍 (ASD) 是一种异质性神经发育障碍,其特征为刻板行为、特定兴趣和沟通技能受损。高水平的促炎细胞因子,如白细胞介素-17A (IL-17A 或 IL-17),被认为是导致这种结果的免疫改变的一部分。在这种情况下,啮齿动物模型有助于阐明 T 细胞激活和 IL-17 分泌在 ASD 发病机制中的作用。关于临床前发现,现有数据在后代中存在矛盾,但在孕鼠中则没有,这表明 IL-17 是一些 ASD 模型中改变行为的主要驱动因素之一,而在其他模型中则没有描述 IL-17 水平的改变。为了弥补这一文献空白,对 ASD 啮齿动物模型中改变的 IL-17 水平进行了系统评价。总共纳入了 28 项探讨 IL-17 水平的研究,观察到这种细胞因子在不同的 ASD 模型中通常增加。本综述中汇编的数据可以帮助选择动物模型来研究细胞因子在 ASD 发展中的作用,以寻求与该疾病患者中观察到的免疫改变的平行关系。

系统评价注册

PROSPERO,标识符 CRD42022306558。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/316a/9226456/ed184e1847a3/fimmu-13-874064-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/316a/9226456/ed184e1847a3/fimmu-13-874064-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/316a/9226456/ed184e1847a3/fimmu-13-874064-g001.jpg

相似文献

1
Aberrant IL-17 Levels in Rodent Models of Autism Spectrum Disorder: A Systematic Review.自闭症谱系障碍啮齿动物模型中异常的白细胞介素-17 水平:系统评价。
Front Immunol. 2022 Jun 10;13:874064. doi: 10.3389/fimmu.2022.874064. eCollection 2022.
2
Maternal IL-17A in autism.自闭症中的母体白细胞介素-17A
Exp Neurol. 2018 Jan;299(Pt A):228-240. doi: 10.1016/j.expneurol.2017.04.010. Epub 2017 Apr 25.
3
Yigansan ameliorates maternal immune activation-induced autism-like behaviours by regulating the IL-17A/TRAF6/MMP9 pathway: Network analysis and experimental validation.益肝散通过调节IL-17A/TRAF6/MMP9通路改善母体免疫激活诱导的自闭症样行为:网络分析与实验验证
Phytomedicine. 2024 Jun;128:155386. doi: 10.1016/j.phymed.2024.155386. Epub 2024 Feb 1.
4
Oral probiotic administration during pregnancy prevents autism-related behaviors in offspring induced by maternal immune activation via anti-inflammation in mice.孕期口服益生菌通过抗炎作用预防母体免疫激活诱导的子代自闭症相关行为。
Autism Res. 2019 Apr;12(4):576-588. doi: 10.1002/aur.2079. Epub 2019 Jan 25.
5
Chronic maternal interleukin-17 and autism-related cortical gene expression, neurobiology, and behavior.母体慢性白细胞介素-17与自闭症相关的皮质基因表达、神经生物学及行为
Neuropsychopharmacology. 2020 May;45(6):1008-1017. doi: 10.1038/s41386-020-0640-0. Epub 2020 Feb 19.
6
Oxidative and inflammatory mediators are upregulated in neutrophils of autistic children: Role of IL-17A receptor signaling.氧化和炎症介质在自闭症儿童的中性粒细胞中上调:IL-17A 受体信号的作用。
Prog Neuropsychopharmacol Biol Psychiatry. 2019 Mar 2;90:204-211. doi: 10.1016/j.pnpbp.2018.12.002. Epub 2018 Dec 6.
7
Immune aberrations in children with Autism Spectrum Disorder: a case-control study from a tertiary care neuropsychiatric hospital in India.自闭症谱系障碍儿童的免疫异常:来自印度一家三级神经精神病医院的病例对照研究。
Psychoneuroendocrinology. 2018 Aug;94:162-167. doi: 10.1016/j.psyneuen.2018.05.002. Epub 2018 May 4.
8
In search of immune cellular sources of abnormal cytokines in the blood in autism spectrum disorder: A systematic review of case-control studies.在自闭症谱系障碍中寻找血液中异常细胞因子的免疫细胞来源:病例对照研究的系统评价。
Front Immunol. 2022 Oct 4;13:950275. doi: 10.3389/fimmu.2022.950275. eCollection 2022.
9
Exogenous IL-17A Alleviates Social Behavior Deficits and Increases Neurogenesis in a Murine Model of Autism Spectrum Disorders.外源性白介素-17A 可减轻自闭症谱系障碍小鼠的社交行为缺陷并增加神经发生。
Int J Mol Sci. 2023 Dec 28;25(1):432. doi: 10.3390/ijms25010432.
10
Behavioral manifestations in rodent models of autism spectrum disorder: protocol for a systematic review and network meta-analysis.自闭症谱系障碍啮齿动物模型中的行为表现:系统评价和网络荟萃分析方案。
Syst Rev. 2022 Jul 26;11(1):150. doi: 10.1186/s13643-022-02028-w.

引用本文的文献

1
Exposure to ambient air pollution over developmental stages induced neurodevelopmental impairment in mice offspring via microbiome-gut-brain axis.在发育阶段暴露于环境空气污染会通过微生物群-肠道-脑轴导致小鼠后代出现神经发育障碍。
Part Fibre Toxicol. 2025 Jul 14;22(1):20. doi: 10.1186/s12989-025-00637-6.
2
Prenatal inflammation impairs early CD11c-positive microglia induction and delays myelination in neurodevelopmental disorders.产前炎症会损害早期CD11c阳性小胶质细胞的诱导,并延缓神经发育障碍中的髓鞘形成。
Commun Biol. 2025 Jan 17;8(1):75. doi: 10.1038/s42003-025-07511-3.
3
Genetically modified animals as models of neurodevelopmental conditions: A review of systematic review reporting quality.

本文引用的文献

1
Maternal gut bacteria drive intestinal inflammation in offspring with neurodevelopmental disorders by altering the chromatin landscape of CD4 T cells.母体肠道细菌通过改变 CD4 T 细胞的染色质景观,驱动伴有神经发育障碍的子代发生肠道炎症。
Immunity. 2022 Jan 11;55(1):145-158.e7. doi: 10.1016/j.immuni.2021.11.005. Epub 2021 Dec 7.
2
Prevalence of Autism Spectrum Disorder and Co-morbidities in Children and Adolescents: A Systematic Literature Review.儿童和青少年自闭症谱系障碍及共病的患病率:一项系统文献综述
Front Psychiatry. 2021 Oct 27;12:744709. doi: 10.3389/fpsyt.2021.744709. eCollection 2021.
3
Exposure to hypertonic solutions during pregnancy induces autism-like behaviors via the NFAT-5 pathway in offspring in a rat model.
作为神经发育疾病模型的转基因动物:系统评价报告质量综述
Brain Neurosci Adv. 2024 Oct 18;8:23982128241287279. doi: 10.1177/23982128241287279. eCollection 2024 Jan-Dec.
4
Gestational hypothyroxinemia induces ASD-like phenotypes in behavior, proinflammatory markers, and glutamatergic protein expression in mouse offspring of both sexes.妊娠甲状腺功能减退症可导致雌雄子代小鼠行为、促炎标志物和谷氨酸能蛋白表达出现 ASD 样表型。
Front Endocrinol (Lausanne). 2024 May 1;15:1381180. doi: 10.3389/fendo.2024.1381180. eCollection 2024.
5
Exogenous IL-17A Alleviates Social Behavior Deficits and Increases Neurogenesis in a Murine Model of Autism Spectrum Disorders.外源性白介素-17A 可减轻自闭症谱系障碍小鼠的社交行为缺陷并增加神经发生。
Int J Mol Sci. 2023 Dec 28;25(1):432. doi: 10.3390/ijms25010432.
6
Advances in the study of IL-17 in neurological diseases and mental disorders.白细胞介素-17在神经疾病和精神障碍研究中的进展
Front Neurol. 2023 Nov 16;14:1284304. doi: 10.3389/fneur.2023.1284304. eCollection 2023.
7
Link between the skin and autism spectrum disorder.皮肤与自闭症谱系障碍之间的联系。
Front Psychiatry. 2023 Oct 18;14:1265472. doi: 10.3389/fpsyt.2023.1265472. eCollection 2023.
8
Combination of machine learning-based bulk and single-cell genomics reveals necroptosis-related molecular subtypes and immunological features in autism spectrum disorder.基于机器学习的 bulk 和单细胞基因组学联合分析揭示自闭症谱系障碍中与坏死性凋亡相关的分子亚型和免疫学特征。
Front Immunol. 2023 Apr 24;14:1139420. doi: 10.3389/fimmu.2023.1139420. eCollection 2023.
9
Poly(I:C)-induced maternal immune activation causes elevated self-grooming in male rat offspring: Involvement of abnormal postpartum static nursing in dam.聚肌胞苷酸诱导的母体免疫激活导致雄性大鼠后代的自我梳理行为增加:与母鼠产后异常静止哺乳有关。
Front Cell Dev Biol. 2023 Mar 16;11:1054381. doi: 10.3389/fcell.2023.1054381. eCollection 2023.
孕期暴露于高渗溶液会通过 NFAT-5 通路在大鼠模型中诱导后代出现自闭症样行为。
Physiol Behav. 2021 Oct 15;240:113545. doi: 10.1016/j.physbeh.2021.113545. Epub 2021 Aug 4.
4
Phenotypic overlap between atopic dermatitis and autism.特应性皮炎与自闭症之间的表型重叠。
BMC Neurosci. 2021 Jun 22;22(1):43. doi: 10.1186/s12868-021-00645-0.
5
Maternal genetics influences fetal neurodevelopment and postnatal autism spectrum disorder-like phenotype by modulating in-utero immunosuppression.母体遗传学通过调节宫内免疫抑制来影响胎儿神经发育和产后自闭症谱系障碍样表型。
Transl Psychiatry. 2021 Jun 5;11(1):348. doi: 10.1038/s41398-021-01472-x.
6
Altered gut microbiome and autism like behavior are associated with parental high salt diet in male mice.肠道微生物组的改变和自闭症样行为与雄性小鼠父母的高盐饮食有关。
Sci Rep. 2021 Apr 16;11(1):8364. doi: 10.1038/s41598-021-87678-x.
7
5-Aminoisoquinolinone, a PARP-1 Inhibitor, Ameliorates Immune Abnormalities through Upregulation of Anti-Inflammatory and Downregulation of Inflammatory Parameters in T Cells of BTBR Mouse Model of Autism.5-氨基异喹啉酮,一种PARP-1抑制剂,通过上调抗炎因子和下调BTBR自闭症小鼠模型T细胞中的炎症参数来改善免疫异常。
Brain Sci. 2021 Feb 17;11(2):249. doi: 10.3390/brainsci11020249.
8
Exposure to Maternal Immune Activation Causes Congenital Unfolded Protein Response Defects and Increases the Susceptibility to Postnatal Inflammatory Stimulation in Offspring.暴露于母体免疫激活会导致先天性未折叠蛋白反应缺陷,并增加后代对产后炎症刺激的易感性。
J Inflamm Res. 2021 Feb 12;14:355-365. doi: 10.2147/JIR.S294238. eCollection 2021.
9
Maternal immune activation in mice disrupts proteostasis in the fetal brain.小鼠母体免疫激活会破坏胎儿大脑中的蛋白质稳态。
Nat Neurosci. 2021 Feb;24(2):204-213. doi: 10.1038/s41593-020-00762-9. Epub 2020 Dec 23.
10
Maternal immune activation induces sustained changes in fetal microglia motility.母体免疫激活诱导胎儿小胶质细胞运动持续改变。
Sci Rep. 2020 Dec 7;10(1):21378. doi: 10.1038/s41598-020-78294-2.