ArticleProceedings of the National Academy of Sciences of the United States of America2015
Amyloid fibrils activate B-1a lymphocytes to ameliorate inflammatory brain disease.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 23 citations in OpenAlex.
- Article
- Antisense oligonucleotides targeting IRF4 alleviate psoriasis.Acta pharmaceutica Sinica. B · 2025Article
- Molecular chaperones in stroke-induced immunosuppression.Neural regeneration research · 2023Article
- Noncanonical B Cells: Characteristics of Uncharacteristic B Cells.Journal of immunology (Baltimore, Md. : 1950) · 2023Review
- Acquired immunity and Alzheimer's disease.Journal of biomedical research · 2022Article
- Understanding the Role of the Gut Microbiome in Brain Development and Its Association With Neurodevelopmental Psychiatric Disorders.Frontiers in cell and developmental biology · 2022Review
- Role of the Cholinergic Anti-Inflammatory Reflex in Central Nervous System Diseases.International journal of molecular sciences · 2021Review
- Tau at the interface between neurodegeneration and neuroinflammation.Genes and immunity · 2020Review
- Development of a brain-permeable peptide nanofiber that prevents aggregation of Alzheimer pathogenic proteins.PloS one · 2020Article
- Amyloid beta is an early responder cytokine and immunopeptide of the innate immune system.Alzheimer's & dementia (New York, N. Y.) · 2020Article
- Hematopoietic stem cell-independent hematopoiesis and the origins of innate-like B lymphocytes.Development (Cambridge, England) · 2019Review
- Sex-specific Tau methylation patterns and synaptic transcriptional alterations are associated with neural vulnerability during chronic neuroinflammation.Journal of autoimmunity · 2019Article
- 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
- Interplay Between the Unfolded Protein Response and Immune Function in the Development of Neurodegenerative Diseases.Frontiers in immunology · 2018Review
- B-1a Cell Development in Splenectomized Neonatal Mice.Frontiers in immunology · 2018Article
- An amyloidogenic hexapeptide derived from amylin attenuates inflammation and acute lung injury in murine sepsis.PloS one · 2018Article
- A Journey in Science: The Privilege of Exploring the Brain and the Immune System.Molecular medicine (Cambridge, Mass.) · 2016Article
- Profile of Lawrence Steinman.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Amyloid fibrils composed of peptides as short as six amino acids are therapeutic in experimental autoimmune encephalomyelitis (EAE), reducing paralysis and inflammation, while inducing several pathways of immune suppression. Intraperitoneal injection of fibrils selectively activates B-1a lymphocytes and two populations of resident macrophages (MΦs), increasing IL-10 production, and triggering their exodus from the peritoneum. The importance of IL-10-producing B-1a cells in this effective therapy was established in loss-of-function experiments where neither B-cell-deficient (μMT) nor IL10(-/-) mice with EAE responded to the fibrils. In gain-of-function experiments, B-1a cells, adoptively transferred to μMT mice with EAE, restored their therapeutic efficacy when Amylin 28-33 was administered. Stimulation of adoptively transferred bioluminescent MΦs and B-1a cells by amyloid fibrils resulted in rapid (within 60 min of injection) trafficking of both cell types to draining lymph nodes. Analysis of gene expression indicated that the fibrils activated the CD40/B-cell receptor pathway in B-1a cells and induced a set of immune-suppressive cell-surface proteins, including BTLA, IRF4, and Siglec G. Collectively, these data indicate that the fibrils activate B-1a cells and F4/80(+) MΦs, resulting in their migration to the lymph nodes, where IL-10 and cell-surface receptors associated with immune-suppression limit antigen presentation and T-cell activation. These mechanisms culminate in reduction of paralytic signs of EAE.
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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.