ArticleKidney international2018
TACI deletion protects against progressive murine lupus nephritis induced by BAFF overexpression.
Article in Kidney international, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 19 citations in OpenAlex.
- BAFF and APRIL Receptors in B Cell Immunity and Autoimmunity.Immunological reviews · 2026Review
- Effect of PET-MPs exposure on the toxicology of PCOS: a multi-platform computational toxicology investigation.Molecular diversity · 2026Article
- Single-cell profiling unveils nephritis-related circulating immunological signatures in systemic lupus erythematosus patients.Communications biology · 2026Article
- The Pathogenesis of Nephrotic Syndrome: A Perspective from B Cells.Kidney diseases (Basel, Switzerland) · 2024Review
- Lymphocytes Change Their Phenotype and Function in Systemic Lupus Erythematosus and Lupus Nephritis.International journal of molecular sciences · 2024Review
- Recent advances in immunotherapies for lupus nephritis.Pediatric nephrology (Berlin, Germany) · 2023Review
- Renal Tissue Expression of BAFF and BAFF Receptors Is Associated with Proliferative Lupus Nephritis.Journal of clinical medicine · 2022Article
- Targeting of EIF4EBP1 by miR-99a-3p affects the functions of B lymphocytes via autophagy and aggravates SLE disease progression.Journal of cellular and molecular medicine · 2021Article
- TACI haploinsufficiency protects against BAFF-driven humoral autoimmunity in mice.European journal of immunology · 2021Article
- B Cells in Systemic Lupus Erythematosus: From Disease Mechanisms to Targeted Therapies.Rheumatic diseases clinics of North America · 2021Review
- Regnase-1 is essential for B cell homeostasis to prevent immunopathology.The Journal of experimental medicine · 2021Article
- Expression of BAFF and BAFF receptors in primary Sjögren's syndrome patients with ectopic germinal center-like structures.Clinical and experimental medicine · 2020Article
- B Cell Abnormalities in Systemic Lupus Erythematosus and Lupus Nephritis-Role in Pathogenesis and Effect of Immunosuppressive Treatments.International journal of molecular sciences · 2019Review
- BAFF inhibition in SLE-Is tolerance restored?Immunological reviews · 2019Review
- Integrated B Cell, Toll-like, and BAFF Receptor Signals Promote Autoantibody Production by Transitional B Cells.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- Interleukin-33 Contributes Toward Loss of Tolerance by Promoting B-Cell-Activating Factor of the Tumor-Necrosis-Factor Family (BAFF)-Dependent Autoantibody Production.Frontiers in immunology · 2018Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
B cells are known to promote the pathogenesis of systemic lupus erythematosus (SLE) via the production of pathogenic anti-nuclear antibodies. However, the signals required for autoreactive B cell activation and the immune mechanisms whereby B cells impact lupus nephritis pathology remain poorly understood. The B cell survival cytokine B cell activating factor of the TNF Family (BAFF) has been implicated in the pathogenesis of SLE and lupus nephritis in both animal models and human clinical studies. Although the BAFF receptor has been predicted to be the primary BAFF family receptor responsible for BAFF-driven humoral autoimmunity, in the current study we identify a critical role for signals downstream of Transmembrane Activator and CAML Interactor (TACI) in BAFF-dependent lupus nephritis. Whereas transgenic mice overexpressing BAFF develop progressive membranoproliferative glomerulonephritis, albuminuria and renal dysfunction, TACI deletion in BAFF-transgenic mice provided long-term (about 1 year) protection from renal disease. Surprisingly, disease protection in this context was not explained by complete loss of glomerular immune complex deposits. Rather, TACI deletion specifically reduced endocapillary, but not mesangial, immune deposits. Notably, although excess BAFF promoted widespread breaks in B cell tolerance, BAFF-transgenic antibodies were enriched for RNA- relative to DNA-associated autoantigen reactivity. These RNA-associated autoantibody specificities were specifically reduced by TACI or Toll-like receptor 7 deletion. Thus, our study provides important insights into the autoantibody specificities driving proliferative lupus nephritis, and suggests that TACI inhibition may be novel and effective treatment strategy in lupus nephritis.
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Registered trials
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