ArticleFrontiers in neuroscience2025
Interleukin-6-induced neuroinflammation is exacerbated by subclinical levels of interferon-α.
Article in Frontiers in neuroscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: Cerebral cytokinopathies are key examples of dysregulated cytokine responses. While mouse models with targeted production of individual cytokines have been pivotal in establishing a causal link between cytokines and disease- especially in the central nervous system-they often fail to replicate the complex inflammatory environments seen in various neuropathological conditions, such as neuromyelitis optica spectrum disorder, where multiple cytokines are upregulated. Methods: To address this, we developed a novel mouse model, GFAP-IL6-IFN Results: Our findings reveal that chronic, low-level production of IFN-α, below the typical disease-inducing threshold, significantly accelerates disease progression in GFAP-IL6-IFN Conclusion: In summary, we demonstrate that subclinical levels of IFN-α can markedly exacerbate IL-6-mediated neurological disease, suggesting that future studies, should consider the combined effects of IL-6 and IFN-α.
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