ArticleJournal of neuroinflammation2022
IL-27 shapes the immune properties of human astrocytes and their impact on encountered human T lymphocytes.
Article in Journal of neuroinflammation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 17 citations in OpenAlex.
- Characterization of an isogenicInfection and immunity · 2026Article
- The Role of Interleukin-18 After Spinal Cord Injury: Mechanisms and Therapeutic Potential.Cells · 2026Review
- Astrocyte Functional Heterogeneity in Multiple Sclerosis.Journal of clinical neurology (Seoul, Korea) · 2026Review
- Targeted inhibition of RGS19 alleviates renal fibrosis by restoring autophagy and modulating immune cell infiltration.Journal of nanobiotechnology · 2026Article
- T cell acute lymphoblastic leukemia exploits a neural proinflammatory pathway to colonize the meninges.The Journal of clinical investigation · 2026Article
- Exploratory study of peripheral immune changes associated with diffusion MRI multi-compartment model in temporal lobe epilepsy.Epilepsia · 2025Article
- Activity and Heterogeneity of Astrocytes in Neurological Diseases: Molecular Mechanisms and Therapeutic Targets.MedComm · 2025Review
- Glial Cells as Key Regulators in Neuroinflammatory Mechanisms Associated with Multiple Sclerosis.International journal of molecular sciences · 2024Review
- Evaluating CXCL12 for Effects on Reactive Gene Expression in Primary Astrocytes.Journal of molecular neuroscience : MN · 2024Article
- Astrocyte KDM4A mediates chemokines and drives neutrophil infiltration to aggravate cerebral ischemia and reperfusion injury.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024Article
- Interleukin 27, like interferons, activates JAK-STAT signaling and promotes pro-inflammatory and antiviral states that interfere with dengue and chikungunya viruses replication in human macrophages.Frontiers in immunology · 2024Article
- The Role of CXCR3 in Nervous System-Related Diseases.Mediators of inflammation · 2024Review
- Bruton's tyrosine kinase-bearing B cells and microglia in neuromyelitis optica spectrum disorder.Journal of neuroinflammation · 2023Article
- Evolutionarily conserved IL-27β enhances Th1 cells potential by triggering the JAK1/STAT1/T-bet axis in Nile tilapia.Fish and shellfish immunology reports · 2023Article
- Classification of T lymphocyte motility behaviors using a machine learning approach.PLoS computational biology · 2023Article
- Article
- Depression Pathophysiology: Astrocyte Mitochondrial Melatonergic Pathway as Crucial Hub.International journal of molecular sciences · 2022Review
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Authors and funding
14 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundInterleukin-27 (IL-27) can trigger both pro- and anti-inflammatory responses. This cytokine is elevated in the central nervous system (CNS) of multiple sclerosis (MS) patients, but how it influences neuroinflammatory processes remains unclear. As astrocytes express the receptor for IL-27, we sought to determine how these glial cells respond to this cytokine and whether such exposure alters their interactions with infiltrating activated T lymphocytes. To determine whether inflammation shapes the impact of IL-27, we compared the effects of this cytokine in non-inflamed and inflamed conditions induced by an IL-1β exposure. MAIN BODY: Transcriptomic analysis of IL-27-exposed human astrocytes showed an upregulation of multiple immune genes. Human astrocytes increased the secretion of chemokines (CXCL9, CXCL10, and CXCL11) and the surface expression of proteins (PD-L1, HLA-E, and ICAM-1) following IL-27 exposure. To assess whether exposure of astrocytes to IL-27 influences the profile of activated T lymphocytes infiltrating the CNS, we used an astrocyte/T lymphocyte co-culture model. Activated human CD4
conclusionOur results establish that IL-27 alters the immune functions of human astrocytes and shapes the profile and motility of encountered T lymphocytes, especially CD8
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