ArticleThe Journal of experimental medicine2021
NK/ILC1 cells mediate neuroinflammation and brain pathology following congenital CMV infection.
Article in The Journal of experimental medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 57 citations in OpenAlex.
- Breaking barriers: how cytomegaloviruses manipulate myeloid cells to invade tissues.EMBO reports · 2026Review
- Metabolomics Highlights Reduced Glutamate and Acetylcarnitine in the Amniotic Fluid of Cytomegalovirus-Infected Pregnant Women.Journal of proteome research · 2026Article
- Persistent microglial activation following neonatal CMV infection mediates neurodegeneration.Science advances · 2026Article
- Acute peritonitis-induced adipose CD127Nature communications · 2026Article
- Microglia in the crosstalk between peripheral and central nervous systems in Parkinson's disease.Translational neurodegeneration · 2025Review
- Molecular features of congenital cytomegalovirus infection in neonatal mouse brain at single-cell resolution.Acta neuropathologica communications · 2025Article
- Predominance of Auditory But Not Vestibular Deficits in a Mouse Model of Congenital Cytomegalovirus Infection.Clinical and experimental otorhinolaryngology · 2025Article
- Neuron-restricted cytomegalovirus latency in the central nervous system regulated by CD4Journal of neuroinflammation · 2025Article
- Shaping the glioblastoma microenvironment to enhance CAR-NK immunotherapy.Frontiers in immunology · 2025Review
- Viral reprogramming of glial metabolism as a driver of neuroinflammation.Frontiers in immunology · 2025Review
- Susceptibility of Mouse Brain to MCMV Infection and Neuroinflammation During Ontogeny.Pathogens (Basel, Switzerland) · 2024Article
- Immune responses drive chorioretinitis and retinal pathology after neonatal CMV infection.Science advances · 2024Article
- Cytomegalovirus infection of the fetal brain: intake of aspirin during pregnancy blunts neurodevelopmental pathogenesis in the offspring.Journal of neuroinflammation · 2024Article
- Cutting Edge: Retinoic Acid Promotes Brain-homing of CD8+ T Cells during Congenital Cytomegalovirus Infection.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Prion protein alters viral control and enhances pathology after perinatal cytomegalovirus infection.Nature communications · 2024Article
- Tissue-specific features of innate lymphoid cells in antiviral defense.Cellular & molecular immunology · 2024Review
- Immune surveillance of cytomegalovirus in tissues.Cellular & molecular immunology · 2024Review
- Cytomegalovirus infection lengthens the cell cycle of granule cell precursors during postnatal cerebellar development.JCI insight · 2024Article
- Comprehensive Analysis of Soluble Mediator Profiles in Congenital CMV Infection Using an MCMV Model.Viruses · 2024Article
- Case report: Autoimmune encephalomyelitis following cytomegalovirus infection after allogeneic hematopoietic stem cell transplantation.Frontiers in medicine · 2024Article
Corrections and comments
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Authors and funding
15 authors at 4 institutions in 4 countries.
Funding
Abstract
Congenital human cytomegalovirus (cHCMV) infection of the brain is associated with a wide range of neurocognitive sequelae. Using infection of newborn mice with mouse cytomegalovirus (MCMV) as a reliable model that recapitulates many aspects of cHCMV infection, including disseminated infection, CNS infection, altered neurodevelopment, and sensorineural hearing loss, we have previously shown that mitigation of inflammation prevented alterations in cerebellar development, suggesting that host inflammatory factors are key drivers of neurodevelopmental defects. Here, we show that MCMV infection causes a dramatic increase in the expression of the microglia-derived chemokines CXCL9/CXCL10, which recruit NK and ILC1 cells into the brain in a CXCR3-dependent manner. Surprisingly, brain-infiltrating innate immune cells not only were unable to control virus infection in the brain but also orchestrated pathological inflammatory responses, which lead to delays in cerebellar morphogenesis. Our results identify NK and ILC1 cells as the major mediators of immunopathology in response to virus infection in the developing CNS, which can be prevented by anti-IFN-γ antibodies.
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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.