ArticleJournal of leukocyte biology2017
Myd88 is required for disease development in a primary Sjögren's syndrome mouse model.
Article in Journal of leukocyte biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 31 citations in OpenAlex.
- MyD88 Deficiency Protects Mice From Experimental Autoimmune Encephalomyelitis by Influencing Both Dendritic Cells and T Cells.Immunology · 2026Article
- IL-36 mediates immune activation in Sjögren's disease and may represent a novel biomarker of disease.Journal of leukocyte biology · 2026Article
- Tlr9 expression protects against Tlr7-dependent exocrine gland and systemic disease manifestations in primary Sjögren's disease in a sex-biased manner.Journal of autoimmunity · 2025Article
- TLR7 activation of age-associated B cells mediates disease in a mouse model of primary Sjögren's disease.Journal of leukocyte biology · 2024Article
- Tlr7 drives sex- and tissue-dependent effects in Sjögren's disease.Frontiers in cell and developmental biology · 2024Article
- Lacrimal Gland Epithelial Cells Shape Immune Responses through the Modulation of Inflammasomes and Lipid Metabolism.International journal of molecular sciences · 2023Article
- Mucosal immunology of the ocular surface.Mucosal immunology · 2022Review
- Bone marrow-derived macrophages from a murine model of Sjögren's syndrome demonstrate an aberrant, inflammatory response to apoptotic cells.Scientific reports · 2022Article
- TLR7 agonism accelerates disease in a mouse model of primary Sjögren's syndrome and drives expansion of T-betFrontiers in immunology · 2022Article
- Nucleic acid-sensing toll-like receptors: Important players in Sjögren's syndrome.Frontiers in immunology · 2022Review
- Research progress on inflammatory mechanism of primary Sjögren syndrome.Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2021Review
- MyD88: At the heart of inflammatory signaling and cardiovascular disease.Journal of molecular and cellular cardiology · 2021Review
- Is there an Inflammation Role for MYD88 in Rheumatoid Arthritis?Inflammation · 2021Article
- Role of the Innate Immunity Signaling Pathway in the Pathogenesis of Sjögren's Syndrome.International journal of molecular sciences · 2021Review
- Tissue-specific activation of Myd88-dependent pathways governs disease severity in primary Sjögren's syndrome.Journal of autoimmunity · 2021Article
- Immune-Intrinsic Myd88 Directs the Production of Antibodies With Specificity for Extracellular Matrix Components in Primary Sjögren's Syndrome.Frontiers in immunology · 2021Article
- TLR7 Signaling Drives the Development of Sjögren's Syndrome.Frontiers in immunology · 2021Article
- Transcriptomic and Single-Cell Analysis Reveals Regulatory Networks and Cellular Heterogeneity in Mouse Primary Sjögren's Syndrome Salivary Glands.Frontiers in immunology · 2021Article
- Arginase 1 is involved in lacrimal hyposecretion in male NOD mice, a model of Sjögren's syndrome, regardless of dacryoadenitis status.The Journal of physiology · 2020Article
- Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Sjögren's syndrome (SS) is an autoimmune disease that often results in diminished exocrine gland function. SS patients also experience systemic disease manifestations, including hypergammaglobulinemia and pulmonary and renal pathoses. MyD88 is a ubiquitously expressed adaptor molecule used by all immune cells that is required for IL-1 receptor (IL-1R), IL-18R, and most TLR signaling. The precise role of MyD88 in SS has not been evaluated, although this adaptor is critical for development of lupus, a related autoimmune disease. This study tested the hypothesis that Myd88-mediated signaling is required for local and systemic SS manifestations. To this end, we generated NOD.B10Sn-
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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.