ArticleJournal of neuroscience research2005
Astrocyte expression of a dominant-negative interferon-gamma receptor.
Article in Journal of neuroscience research, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
10 citing papers in PubMed, 11 citations in OpenAlex.
- Blockade of sustained tumor necrosis factor in a transgenic model of progressive autoimmune encephalomyelitis limits oligodendrocyte apoptosis and promotes oligodendrocyte maturation.Journal of neuroinflammation · 2018Article
- Sustained TNF production by central nervous system infiltrating macrophages promotes progressive autoimmune encephalomyelitis.Journal of neuroinflammation · 2016Article
- Astrocyte response to IFN-γ limits IL-6-mediated microglia activation and progressive autoimmune encephalomyelitis.Journal of neuroinflammation · 2015Article
- Anti-inflammatory mechanisms of IFN-γ studied in experimental autoimmune encephalomyelitis reveal neutrophils as a potential target in multiple sclerosis.Frontiers in neuroscience · 2015Article
- IFN-γ signaling to astrocytes protects from autoimmune mediated neurological disability.PloS one · 2012Article
- Glial cell aquaporin-4 overexpression in transgenic mice accelerates cytotoxic brain swelling.The Journal of biological chemistry · 2008Article
- Role of IFN-gamma responsiveness in CD8 T-cell-mediated viral clearance and demyelination in coronavirus-infected mice.Journal of neuroimmunology · 2008Article
- Article
- Suppressor of cytokine signaling 1 expression protects oligodendrocytes from the deleterious effects of interferon-gamma.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2006Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Interferon-gamma (IFN-gamma) is a major proinflammatory cytokine, and binding to its nearly ubiquitous receptor induces a wide variety of biological functions. To explore the role(s) of IFN-gamma signaling in astrocytes, transgenic mice (GFAP/IFN-gammaR1DeltaIC) expressing a dominant-negative IFN-gamma receptor alpha chain under control of the astrocyte-specific glial fibrillary acid protein (GFAP) promoter were generated. Transgenic mice developed normally, had normal astrocyte numbers and distribution, and exhibited no clinically overt phenotype. Transgene mRNA expression was detected only in the CNS, and the transgene-encoded IFN-gamma receptor 1 colocalized with GFAP, which is consistent with astrocyte expression. Astrocytes from transgenic mice exhibited reduced IFN-gamma-induced signaling as measured by major histocompatibility class II induction. Neither CNS inflammation nor perforin-mediated clearance of a neurotropic mouse hepatitis virus from astrocytes was impaired following infection. Transgenic mice with impaired astrocyte responsiveness to IFN-gamma provide a model for studying the selective astrocyte-dependent effects of this critical cytokine in CNS immunopathology.
Indexed as
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What OpenQuestion holds
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.