ArticleBrain, behavior, and immunity2023
Conserved and cell type-specific transcriptional responses to IFN-γ in the ventral midbrain.
Article in Brain, behavior, and immunity, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 20 citations in OpenAlex.
- Article
- Single-Cell Profiling Reveals Clonally Expanded CX3CR1Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Immune-mediated excitotoxicity in brain disorders.Nature reviews. Immunology · 2026Review
- Th17 effector cytokines induce shared and distinct microglial and endothelial cell responses in a mouse model for post-streptococcal encephalitis.Nature communications · 2026Article
- Tertiary lymphoid structures in neuroinflammation coordinate neuroimmune homeostasis and pathological progression.Journal of neuroinflammation · 2026Review
- Human iPSC-derived neurons stimulated with IFNγ present HLA class I-restricted antigens to cytotoxic CD8Journal of neuroinflammation · 2026Article
- Getting on your last nerve: IFNs and resistance to infection.Journal of immunology (Baltimore, Md. : 1950) · 2026Review
- Molecular Signatures of Id2- and Ascl4-Induced Wiring of Adult Hippocampal Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- Th17 effector cytokines induce shared and distinct microglial and endothelial cell responses in post-streptococcal encephalitis.bioRxiv : the preprint server for biology · 2026Article
- Context matters: Conflicting roles of interferon-γ signaling in CNS diseases.Current opinion in neurobiology · 2026Review
- Glial Cell Dynamics in Neuroinflammation: Mechanisms, Interactions, and Therapeutic Implications.Biomedicines · 2026Review
- Interferon signaling pathways in health and disease.Molecular biomedicine · 2025Review
- Article
- Extracellular tau clearance is governed by its aggregation state and independent of microglial activation by LPS and IFN-γ.Neurobiology of disease · 2025Article
- Article
- Stable Dopamine-Signaling mRNA Co-Expression in the Substantia Nigra Is Deregulated in Pathological Conditions, but Not in Dopamine Transporter Knockout Rats.Biomolecules · 2025Article
- CD8 T cells as drivers of blood-brain barrier disruption.Trends in neurosciences · 2025Review
- Behavioral assessment and gene expression changes in a mouse model with dysfunctional STAT1 signaling.Cell communication and signaling : CCS · 2025Article
- Neurotransmitter and metabolic effects of interferon-alpha in association with decreased striatal dopamine in a non-human primate model of cytokine-Induced depression.Brain, behavior, and immunity · 2025Article
- Toward curing neurological autoimmune disorders: Biomarkers, immunological mechanisms, and therapeutic targets.Neuron · 2025Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Dysregulated inflammation within the central nervous system (CNS) contributes to neuropathology in infectious, autoimmune, and neurodegenerative disease. With the exception of microglia, major histocompatibility complex (MHC) proteins are virtually undetectable in the mature, healthy central nervous system (CNS). Neurons have generally been considered incapable of antigen presentation, and although interferon gamma (IFN-γ) can elicit neuronal MHC class I (MHC-I) expression and antigen presentation in vitro, it has been unclear whether similar responses occur in vivo. Here we directly injected IFN-γ into the ventral midbrain of mature mice and analyzed gene expression profiles of specific CNS cell types. We found that IFN-γ upregulated MHC-I and associated mRNAs in ventral midbrain microglia, astrocytes, oligodendrocytes, and GABAergic, glutamatergic, and dopaminergic neurons. The core set of IFN-γ-induced genes and their response kinetics were similar in neurons and glia, but with a lower amplitude of expression in neurons. A diverse repertoire of genes was upregulated in glia, particularly microglia, which were the only cells to undergo cellular proliferation and express MHC classII (MHC-II) and associated genes. To determine if neurons respond directly via cell-autonomous IFN-γ receptor (IFNGR) signaling, we produced mutant mice with a deletion of the IFN-γ-binding domain of IFNGR1 in dopaminergic neurons, which resulted in a complete loss of dopaminergic neuronal responses to IFN-γ. Our results demonstrate that IFN-γ induces neuronal IFNGR signaling and upregulation of MHC-I and related genes in vivo, although the expression level is low compared to oligodendrocytes, astrocytes, and microglia.
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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.