ArticleProceedings of the National Academy of Sciences of the United States of America2024
IFN-γ-induced Th1-Treg polarization in inflamed brains limits exacerbation of experimental autoimmune encephalomyelitis.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Neuro-immune interactions in tumors, immune-related disorders, and infections.Signal transduction and targeted therapy · 2026Review
- Immune Hallmarks of Recurrent Immune Checkpoint Inhibitor-Mediated Inflammatory Arthritis.Cancer immunology research · 2026Article
- Harnessing Regulatory T Cells to Modulate Acute Brain Injury: From Mechanisms to Therapy.Molecular neurobiology · 2026Review
- IL-33/ST2 Signaling Protects the Heart by Restraining Inflammation and Parasite Burden duringACS infectious diseases · 2026Article
- Increased phenotypic and functional stability of human allospecific induced Tregs is associated with Vitamin C-mediatedFrontiers in immunology · 2026Article
- The Role of IFN-γ-Mediated Immune Cell Crosstalk in the Pathogenesis of Aplastic Anemia.Journal of immunology research · 2026Review
- Treg-derived IFN-γ supports the differentiation of Th1-Treg in tumor immunity and autoimmunity.Frontiers in immunology · 2026Article
- White matter hyperintensities, inflammation and cognitive impairments in drug-naïve first episode schizophrenia patients: a cross-sectional study.BMC psychiatry · 2025Article
- Article
- Single-cell transcriptomics reveals systemic immune dysregulation in non-segmental vitiligo.Frontiers in immunology · 2025Article
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Authors and funding
7 authors.
Funding
Abstract
Experimental autoimmune encephalomyelitis (EAE) is the most widely used rodent model for multiple sclerosis. Interferon-γ (IFN-γ) and regulatory T cells (Tregs) are individually well known to play beneficial roles in amelioration of EAE. However, little is known about the relationship between IFN-γ and Tregs during the disease. Here, we show that IFN-γ polarizes Tregs into T helper 1 (Th1)-type Tregs (Th1-Tregs) to recover from EAE. Single-cell RNA sequencing analysis revealed that brain Tregs showed signs of IFN-γ stimulation during EAE. Loss of IFN-γ signaling in Tregs and of T cell-derived IFN-γ impaired the Th1-Treg polarization and worsened the disease. Moreover, selective ablation of Th1-Tregs using an intersectional genetic method promoted proinflammatory features of macrophages in the inflamed brains and exacerbated the EAE. Taken together, our study highlights a critical role of T cell-derived IFN-γ for Th1-Treg polarization in inflamed brain to ameliorate EAE.
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