ArticleThe Journal of experimental medicine2013
Cgnz1 allele confers kidney resistance to damage preventing progression of immune complex-mediated acute lupus glomerulonephritis.
Article in The Journal of experimental medicine, 2013. 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, 47 citations in OpenAlex.
- Defining PI3K Signaling as a Key Regulator of Molecular Heterogeneity and Inflammation in Glomerular Lupus Nephritis.Immune network · 2026Article
- Gasdermin D deficiency aborts myeloid calcium influx to drive granulopoiesis in lupus nephritis.Cell communication and signaling : CCS · 2024Article
- The immunoregulatory roles of non-haematopoietic cells in the kidney.Nature reviews. Nephrology · 2024Review
- Molecular mechanisms governing the progression of nephritis in lupus prone mice and human lupus patients.Frontiers in immunology · 2023Article
- Targeting Bcl6 in the TREX1 D18N murine model ameliorates autoimmunity by modulating T-follicular helper cells and germinal center B cells.European journal of immunology · 2022Article
- IL-23 reshapes kidney resident cell metabolism and promotes local kidney inflammation.The Journal of clinical investigation · 2021Article
- Autoimmune experimental orchitis and chronic glomerulonephritis with end stage renal disease are controlled by Cgnz1 for susceptibility to end organ damage.Clinical immunology (Orlando, Fla.) · 2021Article
- Targeting Regulatory T Cells for Therapy of Lupus Nephritis.Frontiers in pharmacology · 2021Review
- Autoimmunity and organ damage in systemic lupus erythematosus.Nature immunology · 2020Review
- Interactions among glomerulus infiltrating macrophages and intrinsic cells via cytokines in chronic lupus glomerulonephritis.Journal of autoimmunity · 2020Article
- IL233, an IL-2-IL-33 hybrid cytokine induces prolonged remission of mouse lupus nephritis by targeting Treg cells as a single therapeutic agent.Journal of autoimmunity · 2019Article
- Nature of T cell epitopes in lupus antigens and HLA-DR determines autoantibody initiation and diversification.Annals of the rheumatic diseases · 2019Article
- Complement Therapeutics in Autoimmune Disease.Frontiers in immunology · 2019Review
- New insights into the role of renal resident cells in the pathogenesis of lupus nephritis.The Korean journal of internal medicine · 2018Review
- Bim suppresses the development of SLE by limiting myeloid inflammatory responses.The Journal of experimental medicine · 2017Article
- Pathogenesis of proliferative lupus nephritis from a historical and personal perspective.Clinical immunology (Orlando, Fla.) · 2017Review
- Podocyte Activation of NLRP3 Inflammasomes Contributes to the Development of Proteinuria in Lupus Nephritis.Arthritis & rheumatology (Hoboken, N.J.) · 2017Article
- Pathogenesis of Human Systemic Lupus Erythematosus: A Cellular Perspective.Trends in molecular medicine · 2017Review
- T cells and autoimmune kidney disease.Nature reviews. Nephrology · 2017Review
- Dependence of Glomerulonephritis Induction on Novel Intraglomerular Alternatively Activated Bone Marrow-Derived Macrophages and Mac-1 and PD-L1 in Lupus-Prone NZM2328 Mice.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 3 countries.
Funding
Abstract
Cgnz1 and Agnz1 on the distal region of mouse chromosome 1 are associated with chronic glomerulonephritis (cGN) and acute GN (aGN). NZM2328.Lc1R27 (R27) was generated by introgressing a C57L/J region where Cgnz1 is located to NZM2328. R27 female mice developed aGN mediated by immune complex (IC) deposition and complement activation without progression to cGN with severe proteinuria. End stage renal disease (ESRD) was not seen in R27 mice as old as 15 mo. Thus, aGN and cGN are under separate genetic control, and IC-mediated proliferative GN need not progress to cGN and ESRD. NZM2328 and R27 female mice have comparable immune and inflammatory parameters. In contrast to NZM2328, R27 mice were resistant to sheep anti-mouse GBM serum-induced nephritis, supporting the hypothesis that aGN is mediated by autoimmunity and resistance to the development of cGN is mediated by end organ resistance to damage. Thus, autoimmunity should be considered distinct from end organ damage. The Cgnz1 region has been mapped to a 1.34 MB region with 45 genes. Nine candidate genes were identified. Clinical relevance of these observations is supported by case studies. Clinical implications and the significance to human lupus and other diseases are presented.
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