ArticleJournal of immunology (Baltimore, Md. : 1950)2015
Requirement for Transcription Factor Ets1 in B Cell Tolerance to Self-Antigens.
Article in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 31 citations in OpenAlex.
- IRF4 Promotes Immune Evasion and Shapes the Tumor Microenvironment in Follicular Lymphoma.Blood cancer discovery · 2025Article
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- A dynamic peripheral immune landscape during human pregnancy.Fundamental research · 2025Article
- ETS1 Function in Leukemia and Lymphoma.Advances in experimental medicine and biology · 2024Review
- Toll-like receptors 7 and 9 regulate the proliferation and differentiation of B cells in systemic lupus erythematosus.Frontiers in immunology · 2023Review
- Immune Modulation Using Extracellular Vesicles Encapsulated with MicroRNAs as Novel Drug Delivery Systems.International journal of molecular sciences · 2022Review
- Double-negative (DN) B cells: an under-recognized effector memory B cell subset in autoimmunity.Clinical and experimental immunology · 2021Review
- Combinatorial ETS1-dependent control of oncogenic NOTCH1 enhancers in T-cell leukemia.Blood cancer discovery · 2020Article
- Role of ETS1 in the Transcriptional Network of Diffuse Large B Cell Lymphoma of the Activated B Cell-Like Type.Cancers · 2020Article
- Self-reactivity on a spectrum: A sliding scale of peripheral B cell tolerance.Immunological reviews · 2019Review
- Extrafollicular responses in humans and SLE.Immunological reviews · 2019Review
- SNP rs4937333 in the miRNA-5003-Binding Site of theFrontiers in genetics · 2019Article
- Article
- MicroRNA-326 Upregulates B Cell Activity and Autoantibody Production in Lupus Disease of MRL/lpr Mice.Molecular therapy. Nucleic acids · 2018Article
- Abnormal B Cell Development in Systemic Lupus Erythematosus: What the Genetics Tell Us.Arthritis & rheumatology (Hoboken, N.J.) · 2018Review
- Genetic immunization with mouse thyrotrophin hormone receptor plasmid breaks self-tolerance for a murine model of autoimmune thyroid disease and Graves' orbitopathy.Clinical and experimental immunology · 2018Article
- Plasma Cell Differentiation Pathways in Systemic Lupus Erythematosus.Frontiers in immunology · 2018Review
- Simulation of the Dynamics of Primary Immunodeficiencies in B Cells.Frontiers in immunology · 2018Article
- Updates in Lupus Genetics.Current rheumatology reports · 2017Review
- High-level intrathymic thyrotrophin receptor expression in thyroiditis-prone mice protects against the spontaneous generation of pathogenic thyrotrophin receptor autoantibodies.Clinical and experimental immunology · 2017Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
The differentiation and survival of autoreactive B cells is normally limited by a variety of self-tolerance mechanisms, including clonal deletion, anergy, and clonal ignorance. The transcription factor c-ets-1 (encoded by the Ets1 gene) has B cell-intrinsic roles in regulating formation of Ab-secreting cells by controlling the activity of Blimp1 and Pax5 and may be required for B cell tolerance to self-antigen. To test this, we crossed Ets1(-/-) mice to two different transgenic models of B cell self-reactivity, the anti-hen egg lysozyme BCR transgenic strain and the AM14 rheumatoid factor transgenic strain. BCR transgenic Ets1(-/-) mice were subsequently crossed to mice either carrying or lacking relevant autoantigens. We found that B cells lacking c-ets-1 are generally hyperresponsive in terms of Ab secretion and form large numbers of Ab-secreting cells even in the absence of cognate Ags. When in the presence of cognate Ag, different responses were noted depending on the physical characteristics of the Ag. We found that clonal deletion of highly autoreactive B cells in the bone marrow was intact in the absence of c-ets-1. However, peripheral B cells lacking c-ets-1 failed to become tolerant in response to stimuli that normally induce B cell anergy or B cell clonal ignorance. Interestingly, high-affinity soluble self-antigen did cause B cells to adopt many of the classical features of anergic B cells, although such cells still secreted Ab. Therefore, maintenance of appropriate c-ets-1 levels is essential to prevent loss of self-tolerance in the B cell compartment.
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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.