ArticleJournal of immunology (Baltimore, Md. : 1950)2009
The lupus susceptibility locus Sle1 breaches peripheral B cell tolerance at the antibody-forming cell and germinal center checkpoints.
Article in Journal of immunology (Baltimore, Md. : 1950), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 37 citations in OpenAlex.
- Lactate bridges mesangial cells to the differentiation of follicular helper T cells in lupus nephritis.Nature communications · 2025Article
- New developments implicating IL-21 in autoimmune disease.Journal of autoimmunity · 2021Review
- Spontaneous germinal centers and autoimmunity.Autoimmunity · 2017Review
- Multiple tolerance defects contribute to the breach of B cell tolerance in New Zealand Black chromosome 1 congenic mice.PloS one · 2017Article
- Germinal centers and autoimmune disease in humans and mice.Immunology and cell biology · 2016Review
- IFN-γ receptor and STAT1 signaling in B cells are central to spontaneous germinal center formation and autoimmunity.The Journal of experimental medicine · 2016Article
- Distinct and synergistic roles of FcγRIIB deficiency and 129 strain-derived SLAM family proteins in the development of spontaneous germinal centers and autoimmunity.Journal of autoimmunity · 2015Article
- TLR7 influences germinal center selection in murine SLE.PloS one · 2015Article
- Defects in Germinal Center Selection in SLE.Frontiers in immunology · 2015Review
- The BAFF/APRIL system in SLE pathogenesis.Nature reviews. Rheumatology · 2014Review
- Germinal center B cell depletion diminishes CD4+ follicular T helper cells in autoimmune mice.PloS one · 2014Article
- The lupus-prone NZM2410/NZW strain-derived Sle1b sublocus alters the germinal center checkpoint in female mice in a B cell-intrinsic manner.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- Analysis of a wild mouse promoter variant reveals a novel role for FcγRIIb in the control of the germinal center and autoimmunity.The Journal of experimental medicine · 2012Article
- Modulating proximal cell signaling by targeting Btk ameliorates humoral autoimmunity and end-organ disease in murine lupus.Arthritis research & therapy · 2012Article
- Activation-induced deaminase contributes to the antibody-independent role of B cells in the development of autoimmunity.Autoimmunity · 2012Article
- Resolve, revise, and relax: the 3 Rs of B cell repertoire adjustment.Immunology letters · 2012Review
- B-cell selection and the development of autoantibodies.Arthritis research & therapy · 2012Review
- BAFF/APRIL inhibition decreases selection of naive but not antigen-induced autoreactive B cells in murine systemic lupus erythematosus.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
- Enforced expression of the apoptosis inhibitor Bcl-2 ablates tolerance induction in DNA-reactive B cells through a novel mechanism.Journal of autoimmunity · 2011Article
- Activation-induced cytidine deaminase and aberrant germinal center selection in the development of humoral autoimmunities.The American journal of pathology · 2011Review
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
We have described a line of V(H) knock-in mice termed HKIR in which the transgenic Igh locus partially encodes "dual-reactive" antichromatin and anti-p-azophenylarsonate (Ars) BCRs. HKIR B cells termed canonical, expressing a particular Vkappa L chain, evade central tolerance by down-regulating BCR levels. Canonical HKIR B cells can be recruited into the primary germinal center (GC) and Ab-forming cell (AFC) compartments via Ars immunization. However, their participation in the GC response rapidly wanes and they do not efficiently contribute to the memory compartment, indicating that they are regulated by a GC tolerance checkpoint. We analyzed the influence of the Sle1 genetic interval, shown to break tolerance of chromatin-reactive B cells, on the behavior of HKIR B cells during the anti-Ars response. Canonical B cells from congenic HKIR.Sle1 mice gave rise to elevated short and long-lived AFC responses, and the attenuated GC and memory responses characteristic of these B cells were relieved in adoptive, wild-type recipients. HKIR GC B cells containing Sle1 expressed increased levels of Bcl-2 and c-FLIP and decreased levels of Fas RNA compared with HKIR controls, suggesting direct alteration of the regulation of the GC response by Sle1. High titers of canonical and anti-dsDNA Abs spontaneously developed in many aged HKIR.Sle1 mice. Together, these data indicate that Sle1 perturbs the action of peripheral tolerance checkpoints operative on antinuclear Ag B cells in both the AFC and GC pathways in a cell autonomous fashion.
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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.