ArticleScientific reports2018
Innate IFN-γ ameliorates experimental autoimmune encephalomyelitis and promotes myeloid expansion and PDL-1 expression.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 26 citations in OpenAlex.
- Interferon-γ-induced tolerogenic dendritic cells ameliorate autoimmune neuroinflammation and suppress T-cell responses in multiple sclerosis.Frontiers in immunology · 2026Article
- Synergistic Targeting of Innate Receptors TLR7 and NOD2 for Therapeutic Intervention in Multiple Sclerosis.International journal of molecular sciences · 2024Article
- Article
- The brain cytokine orchestra in multiple sclerosis: from neuroinflammation to synaptopathology.Molecular brain · 2024Review
- Blood immunophenotyping of multiple sclerosis patients at diagnosis identifies a classical monocyte subset associated to disease evolution.Frontiers in immunology · 2024Article
- Advances in immune checkpoint-based immunotherapies for multiple sclerosis: rationale and practice.Cell communication and signaling : CCS · 2023Review
- PD-L1 positive astrocytes attenuate inflammatory functions of PD-1 positive microglia in models of autoimmune neuroinflammation.Nature communications · 2023Article
- Neutrophil biology in injuries and diseases of the central and peripheral nervous systems.Progress in neurobiology · 2023Review
- Interferon-gamma ameliorates experimental autoimmune encephalomyelitis by inducing homeostatic adaptation of microglia.Frontiers in immunology · 2023Article
- The immunology of multiple sclerosis.Nature reviews. Immunology · 2022Review
- PD-1/PD-L Axis in Neuroinflammation: New Insights.Frontiers in neurology · 2022Review
- Innate Signaling in the CNS Prevents Demyelination in a Focal EAE Model.Frontiers in neuroscience · 2021Article
- Therapeutic Functions of Stem Cells from Oral Cavity: An Update.International journal of molecular sciences · 2020Review
- Innate signaling within the central nervous system recruits protective neutrophils.Acta neuropathologica communications · 2020Article
- 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
- Development and applications of a monoclonal antibody against caprine interferon-gamma.BMC biotechnology · 2019Article
- Predictive value of plasmacytoid dendritic cells and Toll-like receptor-9 regarding the treatment efficacy of interferon-α in HBeAg-positive chronic hepatitis B patients.Experimental and therapeutic medicine · 2019Article
- MIS416 Enhances Therapeutic Functions of Human Umbilical Cord Blood-Derived Mesenchymal Stem Cells Against Experimental Colitis by Modulating Systemic Immune Milieu.Frontiers in immunology · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The innate immune system plays a central role in the immune-mediated pathology of multiple sclerosis, and is a therapeutic target for progressive disease. Recently, it has been demonstrated that MIS416, a novel immunomodulatory microparticle that activates NOD-2 and TLR-9-signaling, has disease-modifying activity in multiple sclerosis models. This activity is dependent on innate IFN-γ; however, the precise immune regulatory mechanisms amplified by MIS416 have not previously been determined. Using the experimental autoimmune encephalomyelitis model, MIS416 treatment was associated with IFN-γ-dependant expansion of Treg number and increased suppressive function; however, these cells did not account for disease reduction. Additionally, MIS416 treatment stimulated increased nitric oxide production that was IFN-γ-dependant but dispensable for protection. Finally, MIS416-mediated protection was shown to correlate with IFN-γ-dependant expansion of PDL-1-expressing peripheral myeloid cells, a subset of which was found to be selectively recruited to the brain. This central nervous system trafficking was independent of neuro-inflammatory signals as it occurred in MIS416-treated healthy mice. Together, these findings provide insight into regulatory myeloid cell activities amplified by MIS416-mediated NOD-2 and TLR-9 signalling and highlight the potential importance of these cells in accessing the brain where they may act locally and contribute to the control of neuroinflammation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.