ArticleScientific reports2018
MyD88 signaling causes autoimmune sialadenitis through formation of high endothelial venules and upregulation of LTβ receptor-mediated signaling.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- MyD88 Deficiency Protects Mice From Experimental Autoimmune Encephalomyelitis by Influencing Both Dendritic Cells and T Cells.Immunology · 2026Article
- Salivary gland transcriptomic analysis and immunophenotyping in the IL-14α transgenic mouse model of Sjögren's disease.Frontiers in dental medicine · 2025Article
- Regulation, Maintenance, and Remodeling of High Endothelial Venules in Homeostasis, Inflammation, and Cancer.Current opinion in physiology · 2023Article
- Ectopic lymphoid structures in the aged lacrimal glands.Clinical immunology (Orlando, Fla.) · 2023Article
- Nucleic acid-sensing toll-like receptors: Important players in Sjögren's syndrome.Frontiers in immunology · 2022Review
- Article
- PI3K/AKT/mTOR and TLR4/MyD88/NF-κB Signaling Inhibitors Attenuate Pathological Mechanisms of Allergic Asthma.Inflammation · 2021Article
- TLR7 Signaling Drives the Development of Sjögren's Syndrome.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
- SPOP promotes ubiquitination and degradation of MyD88 to suppress the innate immune response.PLoS pathogens · 2020Article
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
Abstract
Autoimmune sialadenitis (AS), chronic inflammation of the salivary glands (SGs) with focal lymphocyte infiltration, appears in autoimmune diseases such as Sjӧgren's syndrome. The pathological role of MyD88-dependent innate immune signaling in autoimmune diseases including AS has been studied using mouse models, such as NOD mice. Although AS development in NOD mice was reported to be suppressed by Myd88 deficiency, its specific role remains unclear. Here, we determined the potent suppressive effects of Myd88 deficiency on AS development in lupus-prone B6/lpr mice, which have lymphoproliferation abnormalities, and also in NOD mice, which have no lymphoproliferation abnormalities. This indicates that MyD88 signaling triggers AS through both lymphoproliferation-dependent and -independent mechanisms. To address the MyD88-dependent lymphoproliferation-independent AS manifestation, SGs from C57BL/6 mice were analyzed. Remarkable upregulation of Glycam1 and high endothelial venule (HEV)-associated changes were unexpectedly found in Myd88
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