ArticleJournal of autoimmunity2021
Tissue-specific activation of Myd88-dependent pathways governs disease severity in primary Sjögren's syndrome.
Article in Journal of autoimmunity, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- 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
- Role of toll-like receptors in pulmonary immunity: mechanisms and therapeutic implications.Frontiers in immunology · 2025Review
- 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
- TLR7 agonism accelerates disease in a mouse model of primary Sjögren's syndrome and drives expansion of T-betFrontiers in immunology · 2022Article
- The m6A methylation profiles of immune cells in type 1 diabetes mellitus.Frontiers in immunology · 2022Article
- Immune-Intrinsic Myd88 Directs the Production of Antibodies With Specificity for Extracellular Matrix Components in Primary 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
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Myd88 activation is an important driver of autoimmunity. Primary Sjögren's syndrome (pSS) is an autoimmune disease characterized by exocrine gland dysfunction in combination with serious systemic disease manifestations. Myd88-dependent signaling networks remain incompletely understood in the context of pSS. The objective of this study was to establish the contribution of tissue-specific Myd88 activation to local (exocrine) and systemic pSS manifestations. To this end, we generated two novel conditional knockout pSS mouse models; one lacking Myd88 in hematopoietic cells and a second strain in which Myd88 was deleted in the stromal compartment. Spontaneous production of inflammatory mediators was altered in salivary tissue, and nephritis was diminished in both conditional knockout strains. In contrast, pulmonary inflammation was increased in mice lacking Myd88 in hematopoietic cells and was reduced when Myd88 was ablated in stromal cells. Finally, anti-nuclear autoantibodies (ANAs) were attenuated in pSS mice lacking Myd88 in immune cells. Additionally, the ANA-specific B cell repertoire was skewed in the Myd88-deficient strains. Collectively, these data demonstrate that Myd88 activation in specific cell types is essential for distinct aspects of pSS pathology.
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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 Socratic graph.