ArticleJournal of immunology (Baltimore, Md. : 1950)2013
Prolonged apoptotic cell accumulation in germinal centers of Mer-deficient mice causes elevated B cell and CD4+ Th cell responses leading to autoantibody production.
Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 43 citations in OpenAlex.
- Epigenetic regulation of B cell tolerance and dysfunction in autoimmune disease.Nature reviews. Immunology · 2026Review
- From pathogenesis to therapeutic targeting: new insight into TAM receptors in rheumatoid arthritis.Cell & bioscience · 2025Review
- Heterogeneity of Neutrophils and Immunological Function in Neonatal Sepsis: Analysis of Molecular Subtypes Based on Hypoxia-Glycolysis-Lactylation.Mediators of inflammation · 2025Article
- Tingible body macrophages arise from lymph node-resident precursors and uptake B cells by dendrites.The Journal of experimental medicine · 2023Article
- Characterization of gene expression profiles in the mouse brain after 35 days of spaceflight mission.NPJ microgravity · 2022Article
- The TAM receptor tyrosine kinases Axl and Mer drive the maintenance of highly phagocytic macrophages.Frontiers in immunology · 2022Article
- Defective Efferocytosis in a Murine Model of Sjögren's Syndrome Is Mediated by Dysfunctional Mer Tyrosine Kinase Receptor.International journal of molecular sciences · 2021Article
- Role of Gas6 and TAM Receptors in the Identification of Cardiopulmonary Involvement in Systemic Sclerosis and Scleroderma Spectrum Disorders.Disease markers · 2020Observational
- How macrophages deal with death.Nature reviews. Immunology · 2019Review
- Selenium supplementation suppresses immunological and serological features of lupus in B6.Sle1b mice.Autoimmunity · 2019Article
- Gas6/TAM Receptors in Systemic Lupus Erythematosus.Disease markers · 2019Review
- Efferocytosis and autoimmune disease.International immunology · 2018Review
- Lupus-like autoimmune disease caused by a lack of Xkr8, a caspase-dependent phospholipid scramblase.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Pathways leading to an immunological disease: systemic lupus erythematosus.Rheumatology (Oxford, England) · 2017Review
- Spontaneous germinal centers and autoimmunity.Autoimmunity · 2017Review
- The Peyer's Patch Mononuclear Phagocyte System at Steady State and during Infection.Frontiers in immunology · 2017Review
- The Role of TAM Family Receptors in Immune Cell Function: Implications for Cancer Therapy.Cancers · 2016Review
- Concise Review: Mechanisms Behind Apoptotic Cell-Based Therapies Against Transplant Rejection and Graft versus Host Disease.Stem cells (Dayton, Ohio) · 2016Review
- Lupus erythematosus revisited.Seminars in immunopathology · 2016Review
- Increased soluble phagocytic receptors sMer, sTyro3 and sAxl and reduced phagocytosis in juvenile-onset systemic lupus erythematosus.Pediatric rheumatology online journal · 2015Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Mer receptor tyrosine kinase is a member of the Tyro-3/Axl/Mer (TAM) subfamily of receptor tyrosine kinases, and its expression on phagocytes facilitates their clearance of apoptotic cells (ACs). Mer expression in germinal centers (GCs) occurs predominantly on tingible body macrophages. B and T cells do not express Mer. In this study, we show that Mer deficiency ((Mer(-/-)) resulted in the long-term accumulation of ACs primarily in GCs and not in the T cell zone, marginal zone, or red pulp areas of the spleen. AC accumulation in GCs led to augmented Ab-forming cell, GC, and IgG2 Ab responses in Mer(-/-) mice, which were sustained for at least 80 d. Enhanced responses in Mer(-/-) mice were due to increased activation and proliferation of B cells and CD4(+) Th cells, including follicular helper T cells, which resulted in high titers of anti-nuclear Abs in Mer(-/-) mice compared with wild-type controls. Secondary IgG-producing Ab-forming cell, total IgG, and IgG2 Ab responses were also increased in Mer(-/-) mice. Finally, compared with wild-type controls, Mer(-/-) mice had increased percentage of IFN-γ-producing CD4(+) Th cells and elevated levels of Th1 (i.e., IL-2 and IFN-γ) and proinflammatory (i.e., TNF and IL-6) cytokines, consistent with elevated levels of Th1-biased IgG2 Abs in Mer(-/-) mice. Together, our results demonstrate that Mer deficiency induces prolonged accumulation of ACs in GCs, resulting in dysregulation of GC B cell and CD4(+) Th cell responses and Th1 cytokine production, leading to alteration of B cell tolerance and the development of autoantibodies.
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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.