ArticleBiomaterials2017
Polyplexes assembled from self-peptides and regulatory nucleic acids blunt toll-like receptor signaling to combat autoimmunity.
Article in Biomaterials, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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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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
32 citing papers in PubMed, 53 citations in OpenAlex.
- Integrating molecular dynamics simulations to enable rational assembly of immune signals for immunotherapy.Nanoscale horizons · 2026Article
- Antioxidant Polymeric and Non-Polymeric Nanoformulations for the Treatment of Autoimmune Diseases.Current issues in molecular biology · 2026Review
- CRISPR-based gene therapy for huntington's disease: current advances and future prospects.Neurogenetics · 2025Review
- Exploiting Unique Features of Microneedles to Modulate Immunity.Advanced materials (Deerfield Beach, Fla.) · 2023Review
- Delivery route considerations for designing antigen-specific biomaterial strategies to combat autoimmunity.Advanced nanobiomed research · 2023Article
- Biomaterial Strategies for Selective Immune Tolerance: Advances and Gaps.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Review
- Impact of disease-modifying therapy on dendritic cells and exploring their immunotherapeutic potential in multiple sclerosis.Journal of neuroinflammation · 2022Review
- Biophysical Properties of Self-Assembled Immune Signals Impact Signal Processing and the Nature of Regulatory Immune Function.Nano letters · 2021Article
- Exploiting Rational Assembly to Map Distinct Roles of Regulatory Cues during Autoimmune Therapy.ACS nano · 2021Article
- Self-Assembly as a Molecular Strategy to Improve Immunotherapy.Accounts of chemical research · 2020Article
- Synergistic Activation of Toll-Like and NOD Receptors by Complementary Antigens as Facilitators of Autoimmune Disease: Review, Model and Novel Predictions.International journal of molecular sciences · 2020Review
- Recent Advances in Antigen-Specific Immunotherapies for the Treatment of Multiple Sclerosis.Brain sciences · 2020Review
- Recombinant Filamentous Bacteriophages Encapsulated in Biodegradable Polymeric Microparticles for Stimulation of Innate and Adaptive Immune Responses.Microorganisms · 2020Article
- Biomaterials as Tools to Decode Immunity.Advanced materials (Deerfield Beach, Fla.) · 2020Review
- Rational Design of Antigen Incorporation Into Subunit Vaccine Biomaterials Can Enhance Antigen-Specific Immune Responses.Frontiers in immunology · 2020Article
- Phage display as a tool for vaccine and immunotherapy development.Bioengineering & translational medicine · 2020Review
- Directing toll-like receptor signaling in macrophages to enhance tumor immunotherapy.Current opinion in biotechnology · 2019Review
- Article
- Designing inorganic nanomaterials for vaccines and immunotherapies.Nano today · 2019Article
- Engineering Biomaterials to Direct Innate Immunity.Advanced therapeutics · 2019Article
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
Abstract
Autoimmune diseases occur when the immune system incorrectly recognizes self-molecules as foreign; in the case of multiple sclerosis (MS), myelin is attacked. Intriguingly, new studies reveal toll-like receptors (TLRs), pathways usually involved in generating immune responses against pathogens, play a significant role in driving autoimmune disease in both humans and animal models. We reasoned polyplexes formed from myelin self-antigen and regulatory TLR antagonists might limit TLR signaling during differentiation of myelin-specific T cells, inducing tolerance by biasing T cells away from inflammatory phenotypes. Complexes were formed by modifying myelin peptide with cationic amino acids to create peptides able to condense the anionic nucleic-acid based TLR antagonist. These immunological polyplexes eliminate synthetic polymers commonly used to condense polyplexes and do not rely on gene expression; however, the complexes mimic key features of traditional polyplexes such as tunable loading and co-delivery. Using these materials and classic polyplex analysis techniques, we demonstrate condensation of both immune signals, protection from enzymatic degradation, and tunable physicochemical properties. We show polyplexes reduce TLR signaling, and in primary dendritic cell and T cell co-culture, reduce myelin-driven inflammation. During mouse models of MS, these tolerogenic polyplexes improve the progression, severity, and incidence of 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.