ArticleJournal of immunology (Baltimore, Md. : 1950)2013
The interdependent, overlapping, and differential roles of type I and II IFNs in the pathogenesis of experimental autoimmune encephalomyelitis.
Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 64 citations in OpenAlex.
- Association of cytokine levels with treatment duration and patient family history in Egyptian multiple sclerosis patients.Scientific reports · 2026Article
- Tyro3 deletion is protective in experimental autoimmune encephalomyelitis.Immunology and cell biology · 2025Article
- RiboTag-based RNA profiling uncovers oligodendroglial lineage-specific inflammation in autoimmune encephalomyelitis: implications for pathogenesis.Journal of neuroinflammation · 2025Article
- Mac-1 regulates disease stage-specific immunosuppression via the nitric oxide pathway in autoimmune disease.Science advances · 2025Article
- Astrocytes in aging.Neuron · 2025Review
- Therapeutic role of interferon-γ in experimental autoimmune encephalomyelitis is mediated through a tolerogenic subset of splenic CD11bJournal of neuroinflammation · 2024Article
- Interferon-γ controls aquaporin 4-specific Th17 and B cells in neuromyelitis optica spectrum disorder.Brain : a journal of neurology · 2024Article
- Article
- Transforming growth factor receptor III (Betaglycan) regulates the generation of pathogenic Th17 cells in EAE.Frontiers in immunology · 2023Article
- Interferon-gamma ameliorates experimental autoimmune encephalomyelitis by inducing homeostatic adaptation of microglia.Frontiers in immunology · 2023Article
- The interplay between T helper cells and brain barriers in the pathogenesis of multiple sclerosis.Frontiers in cellular neuroscience · 2023Review
- Metabolic regulation and function of T helper cells in neuroinflammation.Seminars in immunopathology · 2022Review
- The role of type I IFN in autoimmune and autoinflammatory diseases with CNS involvement.Frontiers in neurology · 2022Review
- Bidirectional Effect of IFN-γ on Th17 Responses in Experimental Autoimmune Uveitis.Frontiers in ophthalmology · 2022Article
- Cystatin C Plays a Sex-Dependent Detrimental Role in Experimental Autoimmune Encephalomyelitis.Cell reports · 2020Article
- GRIM-19 Ameliorates Multiple Sclerosis in a Mouse Model of Experimental Autoimmune Encephalomyelitis with Reciprocal Regulation of IFNγ/Th1 and IL-17A/Th17 Cells.Immune network · 2020Article
- c-Jun N-Terminal Kinase as a Therapeutic Target in Experimental Autoimmune Encephalomyelitis.Cells · 2020Article
- The impact of regional astrocyte interferon-γ signaling during chronic autoimmunity: a novel role for the immunoproteasome.Journal of neuroinflammation · 2020Article
- Pathogenic T cell cytokines in multiple sclerosis.The Journal of experimental medicine · 2020Review
- Interferon-γ/Interleukin-27 Axis Induces Programmed Death Ligand 1 Expression in Monocyte-Derived Dendritic Cells and Restores Immune Tolerance in Central Nervous System Autoimmunity.Frontiers in immunology · 2020Article
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Type I IFNs (IFN-α and IFN-β) and type II IFN (IFN-γ) mediate both regulation and inflammation in multiple sclerosis, neuromyelitis optica, and in experimental autoimmune encephalomyelitis (EAE). However, the underlying mechanism for these Janus-like activities of type I and II IFNs in neuroinflammation remains unclear. Although endogenous type I IFN signaling provides a protective response in neuroinflammation, we find that when IFN-γ signaling is ablated, type I IFNs drive inflammation, resulting in exacerbated EAE. IFN-γ has a disease stage-specific opposing function in EAE. Treatment of mice with IFN-γ during the initiation phase of EAE leads to enhanced severity of disease. In contrast, IFN-γ treatment during the effector phase attenuated disease. This immunosuppressive activity of IFN-γ required functional type I IFN signaling. In IFN-α/β receptor-deficient mice, IFN-γ treatment during effector phase of EAE exacerbated disease. Using an adoptive transfer EAE model, we found that T cell-intrinsic type I and II IFN signals are simultaneously required to establish chronic EAE by encephalitogenic Th1 cells. However, in Th17 cells loss of either IFN signals leads to the development of a severe chronic disease. The data imply that type I and II IFN signals have independent but nonredundant roles in restraining encephalitogenic Th17 cells in vivo. Collectively, our data show that type I and II IFNs function in an integrated manner to regulate pathogenesis in EAE.
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