ArticlePloS one2014
Targeting innate receptors with MIS416 reshapes Th responses and suppresses CNS disease in a mouse model of multiple sclerosis.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.
- Role of Inflammasomes in Neuroimmune and Neurodegenerative Diseases: A Systematic Review.Mediators of inflammation · 2018Pooled it
- Neutrophils as regulators of macrophage-induced inflammation in a setting of allogeneic bone marrow transplantation.Stem cell reports · 2022Article
- PD-1/PD-L Axis in Neuroinflammation: New Insights.Frontiers in neurology · 2022Review
- NOD-like receptors in autoimmune diseases.Acta pharmacologica Sinica · 2021Review
- Failed, Interrupted, or Inconclusive Trials on Immunomodulatory Treatment Strategies in Multiple Sclerosis: Update 2015-2020.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2020Review
- First-in-human phase I clinical trial of the NY-ESO-1 protein cancer vaccine with NOD2 and TLR9 stimulants in patients with NY-ESO-1-expressing refractory solid tumors.Cancer immunology, immunotherapy : CII · 2020Article
- Innate signaling within the central nervous system recruits protective neutrophils.Acta neuropathologica communications · 2020Article
- The Helminth ParasiteFrontiers in immunology · 2020Article
- Progressive multiple sclerosis: from pathophysiology to therapeutic strategies.Nature reviews. Drug discovery · 2019Review
- Inflammatory Role of TLR-MyD88 Signaling in Multiple Sclerosis.Frontiers in molecular neuroscience · 2019Article
- Review
- Review
- Innate IFN-γ ameliorates experimental autoimmune encephalomyelitis and promotes myeloid expansion and PDL-1 expression.Scientific reports · 2018Article
- 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
- Innate immunity in Sjögren's syndrome.Clinical immunology (Orlando, Fla.) · 2017Review
- Evaluation of neurological changes in secondary progressive multiple sclerosis patients treated with immune modulator MIS416: results from a feasibility study.Pilot and feasibility studies · 2017Article
- A Personalized Approach in Progressive Multiple Sclerosis: The Current Status of Disease Modifying Therapies (DMTs) and Future Perspectives.International journal of molecular sciences · 2016Review
- Reprogramming the Local Lymph Node Microenvironment Promotes Tolerance that Is Systemic and Antigen Specific.Cell reports · 2016Article
- Therapeutic Advances and Future Prospects in Progressive Forms of Multiple Sclerosis.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2016Review
- Advancing drug delivery systems for the treatment of multiple sclerosis.Immunologic research · 2015Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Modification of the innate immune cell environment has recently been recognized as a viable treatment strategy for reducing autoimmune disease pathology. MIS416 is a microparticulate immune response modifier that targets myeloid cells, activating cytosolic receptors NOD2 and TLR9, and has completed a phase 1b/2a trial for the treatment of secondary progressive multiple sclerosis. Using a mouse model of multiple sclerosis, we are investigating the pathways by which activation of TLR9 and NOD2 may modify the innate immune environment and the subsequent T cell-mediated autoimmune responses. We have found that MIS416 has profound effects on the Th subset balance by depressing antigen-specific Th1, Th17, and Th2 development. These effects coincided with an expansion of specific myeloid subpopulations and increased levels of MIS416-stimulated IFN-γ by splenocytes. Additionally, systemic IFN-γ serum levels were enhanced and correlated strongly with disease reduction, and the protective effect of MIS416 was abrogated in IFN-γ-deficient animals. Finally, treatment of secondary progressive MS patients with MIS416 similarly elevated the levels of IFN-γ and IFN-γ-associated proteins in the serum. Together, these studies demonstrate that administration of MIS416, which targets innate cells, reshapes autoimmune T cell responses and leads to a significant reduction in CNS inflammation and disease.
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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.