ArticleThe Journal of clinical investigation2016
Group A Streptococcus intranasal infection promotes CNS infiltration by streptococcal-specific Th17 cells.
Article in The Journal of clinical investigation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.
What it found
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Who cites it
81 citing papers in PubMed, 119 citations in OpenAlex.
- Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal Infections (PANDAS): Autoimmune Mechanisms, Diagnostic Controversies, and Therapeutic Implications.Journal of pediatrics, perinatology and child health · 2026Article
- Th17 effector cytokines induce shared and distinct microglial and endothelial cell responses in a mouse model for post-streptococcal encephalitis.Nature communications · 2026Article
- Infection-Associated Pediatric Acute-Onset Neuropsychiatric Syndrome: A Review of Immunological Mechanisms, Clinical Phenotypes, and Therapeutic Strategies.Infectious disease reports · 2026Review
- Pathology-directed drug delivery strategies: How to overcome blood-brain barrier for the treatment of brain diseases.Acta pharmaceutica Sinica. B · 2026Review
- Th17 effector cytokines induce shared and distinct microglial and endothelial cell responses in post-streptococcal encephalitis.bioRxiv : the preprint server for biology · 2026Article
- The cribriform plate: A dynamic central nervous system-immune hub.The Journal of experimental medicine · 2026Review
- A Case of Ovarian Teratoma-Associated Anti-NMDA Receptor Encephalitis in the Presence of Group A Streptococcus Infection.Case reports in obstetrics and gynecology · 2026Article
- Unbiased autoantibody screening using nucleic acid protein programmable array in pediatric autoimmune neuropsychiatric disorder associated with streptococcal infections.Frontiers in behavioral neuroscience · 2026Article
- Immune dysregulation in pediatric tic disorders: mechanisms, biomarkers, and therapeutic frontiers.Frontiers in immunology · 2026Review
- T cells in Group AFrontiers in cellular and infection microbiology · 2026Review
- Sex-associated and disease state-dependent monocyte polarization and CNS-trafficking phenotypes in pediatric acute-onset neuropsychiatric syndrome (PANS).Journal of neuroinflammation · 2025Article
- Development of a Mouse Model of Coccidioidomycosis Using an Inhalation Exposure System.Journal of fungi (Basel, Switzerland) · 2025Article
- The Immune/Inflammatory Underpinnings of Neurodevelopmental Disorders and Pediatric Acute-Onset Neuropsychiatric Syndrome: A Scoping Review.International journal of molecular sciences · 2025Article
- Neurological Soft Signs at Presentation in Patients With Pediatric Acute-Onset Neuropsychiatric Syndrome.JAMA network open · 2025Article
- Pediatric acute-onset neuropsychiatric syndromes and the gut-oral-brain axis: a narrative review of emerging microbiome-immune interactions and therapeutic perspectives.Frontiers in immunology · 2025Review
- A mini review of the pathogenesis of acute rheumatic fever and rheumatic heart disease.Frontiers in cellular and infection microbiology · 2025Review
- The intricate pathogenicity of Group AVirulence · 2024Review
- Dopamine receptor autoantibody signaling in infectious sequelae differentiates movement versus neuropsychiatric disorders.JCI insight · 2024Article
- Pediatric Acute-Onset Neuropsychiatric Syndrome (PANS) and Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal Infections (PANDAS): Immunological Features Underpinning Controversial Entities.Children (Basel, Switzerland) · 2024Review
- Development of Autoimmune Diseases Among Children With Pediatric Acute-Onset Neuropsychiatric Syndrome.JAMA network open · 2024Article
21 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
Abstract
Group A streptococcal (GAS) infection induces the production of Abs that cross-react with host neuronal proteins, and these anti-GAS mimetic Abs are associated with autoimmune diseases of the CNS. However, the mechanisms that allow these Abs to cross the blood-brain barrier (BBB) and induce neuropathology remain unresolved. We have previously shown that GAS infection in mouse models induces a robust Th17 response in nasal-associated lymphoid tissue (NALT). Here, we identified GAS-specific Th17 cells in tonsils of humans naturally exposed to GAS, prompting us to explore whether GAS-specific CD4+ T cells home to mouse brains following i.n. infection. Intranasal challenge of repeatedly GAS-inoculated mice promoted migration of GAS-specific Th17 cells from NALT into the brain, BBB breakdown, serum IgG deposition, microglial activation, and loss of excitatory synaptic proteins under conditions in which no viable bacteria were detected in CNS tissue. CD4+ T cells were predominantly located in the olfactory bulb (OB) and in other brain regions that receive direct input from the OB. Together, these findings provide insight into the immunopathology of neuropsychiatric complications that are associated with GAS infections and suggest that crosstalk between the CNS and cellular immunity may be a general mechanism by which infectious agents exacerbate symptoms associated with other CNS autoimmune disorders.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.