ArticleProceedings of the National Academy of Sciences of the United States of America2009
Endocytic sequestration of the B cell antigen receptor and toll-like receptor 9 in anergic cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 54 citations in OpenAlex.
- Critical roles of chronic BCR signaling in the differentiation of anergic B cells into age-associated B cells in aging and autoimmunity.Science advances · 2025Article
- Failed Downregulation of PI3K Signaling Makes Autoreactive B Cells Receptive to Bystander T Cell Help.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Type I interferon promotes the fate of Toll-like receptor 9-stimulated follicular B cells to plasma cell differentiation.PNAS nexus · 2024Article
- Factors Governing B Cell Recognition of Autoantigen and Function in Type 1 Diabetes.Antibodies (Basel, Switzerland) · 2024Review
- Asymmetrical forward and reverse developmental trajectories determine molecular programs of B cell antigen receptor editing.Science immunology · 2022Article
- Cellular aspects of the pathogenesis of lupus nephritis.Current opinion in rheumatology · 2021Review
- Antigen Complexed with a TLR9 Agonist Bolsters c-Myc and mTORC1 Activity in Germinal Center B Lymphocytes.ImmunoHorizons · 2019Article
- Silica Exposure Differentially Modulates Autoimmunity in Lupus Strains and Autoantibody Transgenic Mice.Frontiers in immunology · 2019Article
- Altered toll-like receptor responsiveness underlies a dominant heritable defect in B cell tolerance in autoimmune New Zealand Black mice.European journal of immunology · 2018Article
- Igβ ubiquitination activates PI3K signals required for endosomal sorting.The Journal of experimental medicine · 2017Article
- B-cell receptor signaling in diffuse large B-cell lymphoma.Seminars in hematology · 2015Review
- Affinity Inequality among Serum Antibodies That Originate in Lymphoid Germinal Centers.PloS one · 2015Article
- Vimentin is a dominant target of in situ humoral immunity in human lupus tubulointerstitial nephritis.Arthritis & rheumatology (Hoboken, N.J.) · 2014Article
- Synthetic antigens reveal dynamics of BCR endocytosis during inhibitory signaling.ACS chemical biology · 2014Article
- Recruitment of Cbl-b to B cell antigen receptor couples antigen recognition to Toll-like receptor 9 activation in late endosomes.PloS one · 2014Article
- Tolerant anti-insulin B cells are effective APCs.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Robust T-cell stimulation by Epstein-Barr virus-transformed B cells after antigen targeting to DEC-205.Blood · 2013Article
- Receptor cross-talk spatially restricts p-ERK during TLR4 stimulation of autoreactive B cells.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- CD22 and Siglec-G in B cell function and tolerance.Trends in immunology · 2012Review
- Autoreactive preplasma cells break tolerance in the absence of regulation by dendritic cells and macrophages.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 1 country.
Funding
Abstract
In autoimmune prone murine strains, sequential engagement of the B cell antigen receptor (BCR) on the cell surface and toll-like receptors (TLRs) in late endosomes is necessary and sufficient for secretion of autoantibodies. However, ubiquitous nucleoprotein self-antigens fail to elicit productive TLR activation, and break self-tolerance in anergic DNA-reactive B cells. The mechanisms limiting TLR activation in these cells are largely unknown. Here, we demonstrate that in anergic 3H9/Vkappa8 and Ars/A1 B cells the normal endocytic transit of both the ligated BCR and TLR9 into late endosomes is abrogated. The BCR and TLR9 arrest together just outside late endosomes, indicating that they enter this compartment along a single, regulated endocytic route. Access to late endosomes could be restored by reversing anergy through several methods, including conferring genetic susceptibility to autoimmunity, complementing proximal BCR signaling or by preventing BCR binding to self-antigen. Downstream of the BCR, JNK, which is activated in naive but not anergic B cells, regulated entry into late endosomes. Restoration of BCR and TLR9 endocytic trafficking rescued TLR9 activation by BCR-captured ligands. These results indicate that B cell anergy is reinforced by the exclusion of both TLRs and their BCR captured ligands from subcellular environments necessary for TLR activation.
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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.