Interferon γ: a master cytokine in microglia-mediated neural network dysfunction and neurodegeneration
Traditionally, lymphocytic interferon γ (IFN-γ) was considered to be a simple 'booster' of proinflammatory responses by microglia (brain-resident macrophages) during bacterial or viral infection. Recent slice culture (in situ) and in vivo studies suggest, however, that IFN-γ has a unique r...
Gespeichert in:
| Hauptverfasser: | , , |
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| Dokumenttyp: | Article (Journal) |
| Sprache: | Englisch |
| Veröffentlicht: |
22 October 2022
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| In: |
Trends in neurosciences
Year: 2022, Jahrgang: 45, Heft: 12, Pages: 913-927 |
| ISSN: | 1878-108X |
| DOI: | 10.1016/j.tins.2022.10.007 |
| Online-Zugang: | Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1016/j.tins.2022.10.007 Verlag, lizenzpflichtig, Volltext: https://www.sciencedirect.com/science/article/pii/S0166223622002089 
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| Verfasserangaben: | Oliver Kann, Fadi Almouhanna, and Bruno Chausse |
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| 520 | |a Traditionally, lymphocytic interferon γ (IFN-γ) was considered to be a simple 'booster' of proinflammatory responses by microglia (brain-resident macrophages) during bacterial or viral infection. Recent slice culture (in situ) and in vivo studies suggest, however, that IFN-γ has a unique role in microglial activation. Priming by IFN-γ results in proliferation (microgliosis), enhanced synapse elimination, and moderate nitric oxide release sufficient to impair synaptic transmission, gamma rhythm activity, and cognitive functions. Moreover, IFN-γ is pivotal for driving Toll-like receptor (TLR)-activated microglia into neurotoxic phenotypes that induce energetic and oxidative stress, severe network dysfunction, and neuronal death. Pharmacological targeting of activated microglia could be beneficial during elevated IFN-γ levels, blood-brain barrier leakage, and parenchymal T lymphocyte infiltration associated with, for instance, encephalitis, multiple sclerosis, and Alzheimer's disease. | ||
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