ArticleNeurology(R) neuroimmunology & neuroinflammation2026
Interleukin-9 Regulates NF-kB-Mediated Activation of Astrocytes in Multiple Sclerosis Brain.
Article in Neurology(R) neuroimmunology & neuroinflammation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 2 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.
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Who cites it
2 citing papers in PubMed.
- Selected Cytokines and Matrix Metalloproteinases in Pathogenesis and Treatment of Multiple Sclerosis.International journal of molecular sciences · 2026Review
- Interleukin-9 Regulates NF-kB-Mediated Activation of Astrocytes in Multiple Sclerosis Brain.Neurology(R) neuroimmunology & neuroinflammation · 2026Article
Corrections and comments
- Erratum issued
Authors and funding
14 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND AND
objectivesInterleukin-9 (IL-9) is an immune molecule with multiple roles in a variety of cell types. IL-9-induced cell responses are mediated by the IL-9 receptor (IL-9R). Recent evidence demonstrates that expression of IL-9R in post mortem brain tissues of patients with multiple sclerosis (MS) is associated with a protective, anti-inflammatory role of IL-9 in MS. In this study, we investigated the expression of IL-9R in cells resident in the CNS of patients with MS. We found that astrocytes express IL-9R, indicating their expected responsiveness to IL-9. Astrocytes play a critical role in MS, where the inflammatory environment turns them into reactive cells, which actively contribute to the disease. The transcription factor nuclear factor-kB (NF-kB) regulates the response of reactive astrocytes and their potential pathogenic activities during CNS inflammation.
methodsTo address the role of IL-9 in proinflammatory astrocytes, we used 3 different human in vitro models: (1) human astrocytoma cell line (U-373 MG), (2) primary normal human astrocytes, and (3) induced pluripotent stem cell-derived astrocytes. We used interleukin-1β for their conversion into proinflammatory astrocytes.
resultsWe found that IL-9 contributes to the switch of astrocytes from an inflammatory to an anti-inflammatory profile by downregulating NF-kB activation. Moreover, we demonstrated that IL-9 inhibits granulocyte-macrophage colony-stimulating factor (GM-CSF) expression driven by NF-kB. DISCUSSION: Because GM-CSF production by astrocytes is linked to microglial activation and CNS inflammation, these results indicate that IL-9 regulates the astrocyte-microglia axis and has potential therapeutic anti-inflammatory implications in MS.
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