ArticleChildren (Basel, Switzerland)2021
Dysregulation of Ki-67 Expression in T Cells of Children with Autism Spectrum Disorder.
Article in Children (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 15 citations in OpenAlex.
- Altered phenotype and gene expression of regulatory T cells (Tregs) in children with Autism, and the relationship with comorbid gastrointestinal symptoms.Journal of neuroinflammation · 2026Article
- Altered Phenotype and Gene Expression of Regulatory T cells (Tregs) in Children with Autism, and the Relationship with Comorbid Gastrointestinal Symptoms.Research square · 2025Article
- Identification of immune cells and circulating inflammatory factors associated with neurodevelopmental disorders by bidirectional Mendelian randomization and mediation analysis.Scientific reports · 2025Article
- A Systems Biology Approach for Prioritizing ASD Genes in Large or Noisy Datasets.International journal of molecular sciences · 2025Article
- Intervention and research progress of gut microbiota-immune-nervous system in autism spectrum disorders among students.Frontiers in microbiology · 2025Review
- Alterations of the IKZF1-IKZF2 tandem in immune cells of schizophrenia patients regulate associated phenotypes.Journal of neuroinflammation · 2024Article
- Causal effects of 731 immune cell phenotypes on autism spectrum disorder: a Mendelian randomization study.Frontiers in psychiatry · 2024Article
- Review
- Autism and Children: Diagnosis, Functional Profiles and Intervention.Children (Basel, Switzerland) · 2023Article
- Pinocembrin Reduces Keratinocyte Activation and Ameliorates Imiquimod-Induced Psoriasis-like Dermatitis in BALB/c Mice through the Heme Oxygenase-1/Signal Transducer and Activator of Transcription 3 Pathway.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Transcriptomic Analysis of the Mechanisms for Alleviating Psoriatic Dermatitis Using Taodan Granules in an Imiquimod-Induced Psoriasis-like Mouse Model.Frontiers in pharmacology · 2021Article
- Article
- Microbiome-Specific Statistical Modeling Identifies Interplay Between Gastrointestinal Microbiome and Neurobehavioral Outcomes in Patients With Autism: A Case Control Study.Frontiers in psychiatry · 2021Article
- Systems Pharmacology Approach and Experiment Evaluation Reveal Multidimensional Treatment Strategy of LiangXueJieDu Formula for Psoriasis.Frontiers in pharmacology · 2021Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by behavioral abnormalities such as impairments in social function and deficits in communication. The etiology of autism is unknown in most cases, but many studies have pointed towards the immune system as a causative agent in autism. Specific studies implicated lymphocytes, natural killer (NK) cells, monocytes, cytokines, and specific transcription factors in the development of ASD. The protein Ki-67 is n expressed in the proliferating cells and is used as a tool in several disorders. Ki-67 plays a crucial role in many neurological diseases. However, Ki-67 role in ASD is not fully understood. In this study, we investigated the possible role of Ki-67 expression in autistic children. We compared Ki-67 production in CD3+, CD4+, CD8+, CXCR4+, CXCR7+, CD45R+, HLA-DR+, GATA3+, Helios+, and FOXP3+ peripheral blood mononuclear cells (PBMCs) in autistic children to typically developing (TD) controls using immunofluorescence staining. We also determined Ki-67 mRNA levels in PBMCs using RT-PCR. The results revealed that autistic children had significantly increased numbers of CD3+Ki-67+, CD4+Ki-67+, CD8+Ki-67+, CXCR4+Ki-67+, CXCR7+Ki-67+, CD45R+Ki-67+, HLA-DR+Ki-67+, CXCR4+GATA3+, GATA3+Ki-67+ cells and decreased Helios+Ki-67+ and FOXP3+Ki-67+ cells compared with TD controls. In addition, the autistic children showed upregulation of Ki-67 mRNA levels compared with TD controls. Further studies need to be carried out to assess the exact role of Ki-67 and its therapeutic potential in ASD.
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