ArticleJournal of immunology (Baltimore, Md. : 1950)2014
Requirement for MyD88 signaling in B cells and dendritic cells for germinal center anti-nuclear antibody production in Lyn-deficient mice.
Article in Journal of immunology (Baltimore, Md. : 1950), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
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Who cites it
65 citing papers in PubMed, 92 citations in OpenAlex.
- Lyn governs the establishment and maintenance of B cell anergy by suppressing PI3K signaling.Nature communications · 2026Article
- Lyn restrains lupus via kinase-independent mechanisms that limit Toll-like receptor activation and type I interferon responsiveness.Science advances · 2025Article
- 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
- The parasitic worm product ES-62 protects against collagen-induced arthritis by resetting the gut-bone marrow axis in a microbiome-dependent manner.Frontiers in tropical diseases · 2024Article
- The dualistic role of Lyn tyrosine kinase in immune cell signaling: implications for systemic lupus erythematosus.Frontiers in immunology · 2024Review
- Validation of a murine proteome-wide phage display library for identification of autoantibody specificities.JCI insight · 2023Article
- Nucleic acid-triggered tumoral immunity propagates pH-selective therapeutic antibodies through tumor-driven epitope spreading.Cancer science · 2023Article
- Review
- Role of inhibitory signaling in peripheral B cell tolerance.Immunological reviews · 2022Review
- Regulatory strategies limiting endosomal Toll-like receptor activation in B cells.Immunological reviews · 2022Review
- A dominant function of LynB kinase in preventing autoimmunity.Science advances · 2022Article
- The parasitic worm product ES-62 protects the osteoimmunology axis in a mouse model of obesity-accelerated ageing.Frontiers in immunology · 2022Article
- Loss of CD11b Accelerates Lupus Nephritis in Lyn-Deficient Mice Without Disrupting Glomerular Leukocyte Trafficking.Frontiers in immunology · 2022Article
- Induction of Foxp3 and activation of Tregs by HSP gp96 for treatment of autoimmune diseases.iScience · 2021Article
- Integrin CD11b Negatively Regulates B Cell Receptor Signaling to Shape Humoral Response during Immunization and Autoimmunity.Journal of immunology (Baltimore, Md. : 1950) · 2021Article
- B Cells in Systemic Lupus Erythematosus: From Disease Mechanisms to Targeted Therapies.Rheumatic diseases clinics of North America · 2021Review
- Review
- Tissue-specific activation of Myd88-dependent pathways governs disease severity in primary Sjögren's syndrome.Journal of autoimmunity · 2021Article
- Toll-like receptor signalling in B cells during systemic lupus erythematosus.Nature reviews. Rheumatology · 2021Review
- Immune-Intrinsic Myd88 Directs the Production of Antibodies With Specificity for Extracellular Matrix Components in Primary Sjögren's Syndrome.Frontiers in immunology · 2021Article
5 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 3 institutions in 3 countries.
Funding
Abstract
The intracellular tyrosine kinase Lyn mediates inhibitory receptor function in B cells and myeloid cells, and Lyn(-/-) mice spontaneously develop an autoimmune and inflammatory disease that closely resembles human systemic lupus erythematosus. TLR-signaling pathways have been implicated in the production of anti-nuclear Abs in systemic lupus erythematosus and mouse models of it. We used a conditional allele of Myd88 to determine whether the autoimmunity of Lyn(-/-) mice is dependent on TLR/MyD88 signaling in B cells and/or in dendritic cells (DCs). The production of IgG anti-nuclear Abs, as well as the deposition of these Abs in the glomeruli of the kidneys, leading to glomerulonephritis in Lyn(-/-) mice, were completely abolished by selective deletion of Myd88 in B cells, and autoantibody production and glomerulonephritis were delayed or decreased by deletion of Myd88 in DCs. The reduced autoantibody production in mice lacking MyD88 in B cells or DCs was accompanied by a dramatic decrease in the spontaneous germinal center (GC) response, suggesting that autoantibodies in Lyn(-/-) mice may depend on GC responses. Consistent with this view, IgG anti-nuclear Abs were absent if T cells were deleted (TCRβ(-/-) TCRδ(-/-) mice) or if T cells were unable to contribute to GC responses as the result of mutation of the adaptor molecule SAP. Thus, the autoimmunity of Lyn(-/-) mice was dependent on T cells and on TLR/MyD88 signaling in B cells and in DCs, supporting a model in which DC hyperactivity combines with defects in tolerance in B cells to lead to a T cell-dependent systemic autoimmunity in Lyn(-/-) mice.
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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.