ArticleEuropean journal of immunology2008
Systemic autoimmunity in BAFF-R-mutant A/WySnJ strain mice.
Article in European journal of immunology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 22 citations in OpenAlex.
- T cell Dissimilarities in B Cell Activating Factor-Deficient Versus B Cell Activating Factor Receptor 3-Deficient Systemic Lupus Erythematosus-Prone NZM 2328 Mice as Contributors to Their Divergent Clinical Outcomes.ACR open rheumatology · 2024Article
- Prospective Analysis of B Lymphocyte Subtypes, before and after Initiation of Dialysis, in Patients with End-Stage Renal Disease.Life (Basel, Switzerland) · 2023Article
- Association of BAFF with PI3K/Akt/mTOR signaling in lupus nephritis.Molecular medicine reports · 2017Article
- Article
- Historical perspectives on tumor necrosis factor and its superfamily: 25 years later, a golden journey.Blood · 2012Review
- Regulation of B cell activating factor (BAFF) receptor expression by NF-ΚB signaling in rheumatoid arthritis B cells.Experimental & molecular medicine · 2011Article
- Expansion of immunoglobulin-secreting cells and defects in B cell tolerance in Rag-dependent immunodeficiency.The Journal of experimental medicine · 2010Article
- The adaptor molecule Act1 regulates BAFF responsiveness and self-reactive B cell selection during transitional B cell maturation.Journal of immunology (Baltimore, Md. : 1950) · 2010Article
- Effect of end-stage renal disease on B-lymphocyte subpopulations, IL-7, BAFF and BAFF receptor expression.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2010Article
- Murine BAFF-receptor residues 168-175 are essential for optimal CD21/35 expression but dispensable for B cell survival.Molecular immunology · 2009Article
- Altered BAFF-receptor signaling and additional modifier loci contribute to systemic autoimmunity in A/WySnJ mice.European journal of immunology · 2009Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Systemic lupus erythematosis is an autoimmune disease of unknown etiology. Lupus pathology is thought to reflect autoantibody-mediated damage due to a failure of B lymphocyte tolerance. Since excessive B cell-activating factor belonging to the TNF family (BAFF) expression correlates with human and murine lupus, and BAFF signals B cell survival through BAFF-R, it is believed that excessive BAFF-R signaling can subvert B cell tolerance and facilitate lupus development. Here we report the unexpected finding that BAFF-R-mutant A/WySnJ mice develop a lupus-like syndrome. These mice carry the B cell maturation defect-1 (Bcmd-1) mutant allele of the Baffr gene. Bcmd-1 causes premature B cell death and profound B cell deficiency. Despite having 90% fewer splenic B cells than normal mice, A/WySnJ mice had an 18-fold increased frequency of splenocytes secreting IgM antibodies to dsDNA, and increased amounts of circulating IgM and IgG to dsDNA by 9 months of age. By age 11 months, most A/WySnJ mice displayed renal pathology characteristic of lupus, including proteinuria as well as periodic acid-Schiff-positive deposits and glomerular capillary bed destruction. Importantly, we genetically linked this autoimmunity to Bcmd-1, since congenic AW.Baffr(+/+) mice carrying a wild-type allele developed none of these phenotypes. Our data provide the first evidence linking altered BAFF-R signaling to the development of B cell-mediated autoimmunity.
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