ArticleThe Journal of experimental medicine2014
Mechanisms of action of therapeutic amyloidogenic hexapeptides in amelioration of inflammatory brain disease.
Article in The Journal of experimental medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Neutrophils, NETs and multiple sclerosis: a mini review.Frontiers in immunology · 2025Review
- Molecular chaperones in stroke-induced immunosuppression.Neural regeneration research · 2023Article
- Development of a brain-permeable peptide nanofiber that prevents aggregation of Alzheimer pathogenic proteins.PloS one · 2020Article
- Small Heat Shock Proteins, Amyloid Fibrils, and Nicotine Stimulate a Common Immune Suppressive Pathway with Implications for Future Therapies.Cold Spring Harbor perspectives in medicine · 2019Review
- Amyloids in Site-Specific Autoimmune Reactions and Inflammatory Responses.Frontiers in immunology · 2019Review
- Identification of a common immune regulatory pathway induced by small heat shock proteins, amyloid fibrils, and nicotine.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- An amyloidogenic hexapeptide derived from amylin attenuates inflammation and acute lung injury in murine sepsis.PloS one · 2018Article
- APP Regulates Microglial Phenotype in a Mouse Model of Alzheimer's Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- A Journey in Science: The Privilege of Exploring the Brain and the Immune System.Molecular medicine (Cambridge, Mass.) · 2016Article
- Amyloid fibrils activate B-1a lymphocytes to ameliorate inflammatory brain disease.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Amyloid fibrils composed of peptides as short as six amino acids are effective therapeutics for experimental autoimmune encephalomyelitis (EAE). Immunosuppression arises from at least two pathways: (1) expression of type 1 IFN by pDCs, which were induced by neutrophil extracellular traps arising from the endocytosis of the fibrils; and (2) the reduced expression of IFN-γ, TNF, and IL-6. The two independent pathways stimulated by the fibrils can act in concert to be immunosuppressive in Th1 indications, or in opposition, resulting in inflammation when Th17 T lymphocytes are predominant. The generation of type 1 IFN can be minimized by using polar, nonionizable, amyloidogenic peptides, which are effective in both Th1 and Th17 polarized EAE.
Indexed as
Identifiers
What OpenQuestion holds
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.