ArticleProceedings of the National Academy of Sciences of the United States of America2000
Different sensitivity to receptor editing of B cells from mice hemizygous or homozygous for targeted Ig transgenes.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed.
- Genetic background shapes the naïve IgM B cell receptor repertoire in mice.Frontiers in immunology · 2026Article
- Regulation of Foxo1 expression is critical for central B cell tolerance and allelic exclusion.Cell reports · 2024Article
- CD19 Is Internalized Together with IgM in Proportion to B Cell Receptor Stimulation and Is Modulated by Phosphatidylinositol 3-Kinase in Bone Marrow Immature B Cells.ImmunoHorizons · 2023Article
- B-cell intrinsic and extrinsic signals that regulate central tolerance of mouse and human B cells.Immunological reviews · 2022Review
- Transplantation tolerance modifies donor-specific B cell fate to suppress de novo alloreactive B cells.The Journal of clinical investigation · 2020Article
- Cross-Reactive Antigen Expressed by B6 Splenocytes Drives Receptor Editing and Marginal Zone Differentiation of IgG2a-Reactive AM14 Vκ8 B Cells.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- Active PI3K abrogates central tolerance in high-avidity autoreactive B cells.The Journal of experimental medicine · 2019Article
- Cytokine-Producing B Cells Promote Immune-Mediated Bile Duct Injury in Murine Biliary Atresia.Hepatology (Baltimore, Md.) · 2018Article
- Activation of the MEK-ERK Pathway Is Necessary but Not Sufficient for Breaking Central B Cell Tolerance.Frontiers in immunology · 2018Article
- NLR Nod1 signaling promotes survival of BCR-engaged mature B cells through up-regulated Nod1 as a positive outcome.The Journal of experimental medicine · 2017Article
- Humanized Immunoglobulin Mice: Models for HIV Vaccine Testing and Studying the Broadly Neutralizing Antibody Problem.Advances in immunology · 2017Review
- Human Ig knockin mice to study the development and regulation of HIV-1 broadly neutralizing antibodies.Immunological reviews · 2017Review
- Activation of Ras overcomes B-cell tolerance to promote differentiation of autoreactive B cells and production of autoantibodies.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Bruton's tyrosine kinase promotes persistence of mature anti-insulin B cells.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- Direct reduction of antigen receptor expression in polyclonal B cell populations developing in vivo results in light chain receptor editing.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- Negative selection by IgM superantigen defines a B cell central tolerance compartment and reveals mutations allowing escape.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
- Cellular competition independent of BAFF/B lymphocyte stimulator results in low frequency of an autoreactive clonotype in mature polyclonal B cell compartments.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
- B cell receptor editing in tolerance and autoimmunity.Annals of the New York Academy of Sciences · 2011Review
- BAFF receptor signaling aids the differentiation of immature B cells into transitional B cells following tonic BCR signaling.Journal of immunology (Baltimore, Md. : 1950) · 2010Article
- Ras activation of Erk restores impaired tonic BCR signaling and rescues immature B cell differentiation.The Journal of experimental medicine · 2010Article
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3 authors.
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Abstract
Ig knock-in mice have been used to study the relative contribution of receptor selection versus clonal selection in the control of autoreactive B cells. The anti-MHC class I 3-83Ig knock-in (3-83Igi) mice manifest extensive receptor editing in the presence of H-2(b). However, receptor editing is also observed on the H-2(d) background, although reactivity toward this antigen is below detection and its presence does not affect the generation of 3-83Ig(+) mature B cells in classical 3-83Ig transgenic mice. In this study we have analyzed the contribution of genetic background, B cell receptor signaling, and transgene copy number on the initiation and extent of receptor editing in the 3-83Igi;H-2(d) mice. Crossing the 3-83Ig insertion into either CD45-deficient H-2(d) mice or onto the BALB/c background reduces the extent of receptor editing and increases the fraction of 3-83Ig-expressing B cells, indicating that in the original line editing depends on B cell receptor signaling induced by cross-reacting antigen(s). However, receptor editing is still detectable in hemizygous 3-83Igi mice even on the BALB/c background, on which the 3-83 antibody was originally raised, whereas it is abrogated in homozygous 3-83Igi;H-2(d) animals. This latter observation indicates that immature B cells expressing immunoglobulin from single heavy and light chain loci, as they do physiologically, utilize receptor editing for an exquisite quality control of their antigen receptor that may only partly be based on self-reactivity.
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