ArticleEuropean journal of immunology2012
Lyn deficiency affects B-cell maturation as well as survival.
Article in European journal of immunology, 2012. 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.
- 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
- T-independent B-cell effect of agents associated with swine grower-finisher diarrhea.Veterinary research communications · 2024Article
- Single-nuclei transcriptome analysis of channel catfish spleen provides insight into the immunome of an aquaculture-relevant species.PloS one · 2024Article
- Learning cell identity in immunology, neuroscience, and cancer.Seminars in immunopathology · 2023Review
- Role of inhibitory signaling in peripheral B cell tolerance.Immunological reviews · 2022Review
- Computational Prediction of Biomarkers, Pathways, and New Target Drugs in the Pathogenesis of Immune-Based Diseases Regarding Kidney Transplantation Rejection.Frontiers in immunology · 2021Article
- B Cell Development in the Bone Marrow Is Regulated by Homeostatic Feedback Exerted by Mature B Cells.Frontiers in immunology · 2016Article
- Requirement for MyD88 signaling in B cells and dendritic cells for germinal center anti-nuclear antibody production in Lyn-deficient mice.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- B cell-specific loss of Lyn kinase leads to autoimmunity.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Lyn, an Src-family protein tyrosine kinase expressed in B lymphocytes, contributes to initiation of BCR signaling and is also responsible for feedback inhibition of BCR signaling. Lyn-deficient mice have a decreased number of follicular B cells and also spontaneously develop a lupus-like autoimmunity. We used flow cytometric analysis, BrdU labeling and our mathematical models of B-cell population dynamics, to analyze how Lyn deficiency impacts B-cell maturation and survival. We found that Lyn-deficient transitional 1 (T1) cells develop normally, but T2 cells develop primarily from the T1 subset in the spleen and fail to also develop directly from BM immature B cells. Lyn-deficient T2 cells either mature to the follicular B-cell type at a close to normal rate, or die in this compartment rather than access the T3 anergic subset. The ≈ 40% of WT follicular cells that were short-lived exited primarily by joining the T3 anergic subset, whereas the ≈ 15% Lyn(-/-) follicular cells that were not long lived had a high death rate and died in this compartment rather than entering the T3 subset. We hypothesize that exaggerated BCR signaling resulting from weak interactions with self-antigens is largely responsible for these alterations in Lyn-deficient B cells.
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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.