ArticleJournal of immunology (Baltimore, Md. : 1950)2015
Silencing IFN-γ binding/signaling in astrocytes versus microglia leads to opposite effects on central nervous system autoimmunity.
Article in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
51 citing papers in PubMed, 69 citations in OpenAlex.
- Astrocytic-OTUD7B ameliorates murine experimental autoimmune encephalomyelitis by stabilizing glial fibrillary acidic protein and preventing inflammation.Nature communications · 2025Article
- Modeling neuroinflammatory interactions between microglia and astrocytes in a human iPSC-based coculture platform.Cell communication and signaling : CCS · 2025Article
- Cytokine Gene Expression and Treatment Impact on MRI Outcomes in Jordanian Patients with Multiple Sclerosis.Life (Basel, Switzerland) · 2025Article
- RiboTag-based RNA profiling uncovers oligodendroglial lineage-specific inflammation in autoimmune encephalomyelitis: implications for pathogenesis.Journal of neuroinflammation · 2025Article
- Ubiquitination-mediated upregulation of glycolytic enzyme MCT4 in promoting astrocyte reactivity during neuroinflammation.Journal of neuroinflammation · 2025Article
- Adenosine ACell communication and signaling : CCS · 2025Article
- Exploring neuroglial signaling: diversity of molecules implicated in microglia-to-astrocyte neuroimmune communication.Reviews in the neurosciences · 2025Review
- From diagnosis to treatment: exploring the mechanisms underlying optic neuritis in multiple sclerosis.Journal of translational medicine · 2025Review
- Orchestrating Stress Responses in Multiple Sclerosis: A Role for Astrocytic IFNγ Signaling.International journal of molecular sciences · 2024Review
- Positive regulation of Vav1 by Themis controls CD4 T cell pathogenicity in a mouse model of central nervous system inflammation.Cellular and molecular life sciences : CMLS · 2024Article
- Peptide discovery across the spectrum of neuroinflammation; microglia and astrocyte phenotypical targeting, mediation, and mechanistic understanding.Frontiers in molecular neuroscience · 2024Review
- Prolonged STAT1 activation in neurons drives a pathological transcriptional response.Journal of neuroimmunology · 2023Article
- Blocking the IFN-gamma signal in the choroid plexus confers resistance to experimental autoimmune encephalomyelitis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023Article
- Interferon-gamma ameliorates experimental autoimmune encephalomyelitis by inducing homeostatic adaptation of microglia.Frontiers in immunology · 2023Article
- Elucidating the neuroimmunology of traumatic brain injury: methodological approaches to unravel intercellular communication and function.Frontiers in cellular neuroscience · 2023Review
- Tylvalosin Tartrate Improves the Health Status of Swine Herds during Immunization with Porcine Reproductive and Respiratory Syndrome Virus-Inactivated Vaccine.Veterinary sciences · 2022Article
- Palmitoylethanolamide and White Matter Lesions: Evidence for Therapeutic Implications.Biomolecules · 2022Review
- Astrocytes and Inflammatory T Helper Cells: A Dangerous Liaison in Multiple Sclerosis.Frontiers in immunology · 2022Review
- Enriched Environment Effects on Myelination of the Central Nervous System: Role of Glial Cells.Neural plasticity · 2022Review
- NK/ILC1 cells mediate neuroinflammation and brain pathology following congenital CMV infection.The Journal of experimental medicine · 2021Article
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
Abstract
IFN-γ, the hallmark cytokine of Th1 cells, plays an important role in experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis. Thus far, the role of IFN-γ in EAE has been largely studied through its effects on immune cells, whereas much less is known about its effects on CNS cells, especially in vivo. In this study, we dissected the in vivo effects and mechanisms of IFN-γ binding/signaling in astrocytes and microglia, and found that IFN-γ signaling in these cell types has opposite effects in EAE pathogenesis. Silencing IFN-γ binding/signaling in astrocytes alleviated EAE, whereas in microglia, and likely in some infiltrating macrophages, it increased disease severity. Silencing IFN-γ signaling in astrocytes resulted in diminished expression of chemokines and fewer inflammatory cells infiltrating into the CNS, whereas blocking IFN-γ binding/signaling in microglia, probably infiltrating macrophages as well, increased disease severity through augmented activation and proliferation of microglia. Further, blocking IFN-γ binding/signaling in astrocytes alleviated both Th1- and Th17-mediated adoptive EAE, indicating an important role for IFN-γ signaling in astrocytes in autoimmune CNS inflammation. Thus, our study defines novel mechanisms of action of IFN-γ in EAE pathogenesis, and also highlights an opportunity for development of multiple sclerosis therapies directed at CNS cells.
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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.