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Lupus nephritis is an immune-mediated disease, where antibodies and T cells both play pathogenic roles. Since spontaneous lupus nephritis in mouse models takes 6-12 months to manifest, there is an urgent need for a mouse model that can be used to delineate the pathogenic processes that lead to immune nephritis, over a quicker time frame. We propose that the experimental anti-glomerular basement membrane (GBM) disease model might be a suitable tool for uncovering some of the molecular steps underlying lupus nephritis. This article reviews the current evidence that supports the use of the experimental anti-GBM nephritis model for studying spontaneous lupus nephritis. Importantly, out of about 25 different molecules that have been specifically examined in the experimental anti-GBM model and also spontaneous lupus nephritis, all influence both diseases concordantly, suggesting that the experimental model might be a useful tool for unraveling the molecular basis of spontaneous lupus nephritis. This has important clinical implications, both from the perspective of genetic susceptibility as well as clinical therapeutics.
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http://dx.doi.org/10.1016/j.clim.2007.05.007 | DOI Listing |
Curr Opin Immunol
September 2025
Univ. Grenoble Alpes, CNRS, CEA, UMR5075, IBS, Laboratoire d'Immunologie, CHU Grenoble Alpes, Grenoble, France.
The complement system plays a paradoxical role in systemic lupus erythematosus physiopathology, acting both as a protective mechanism and as a driver of tissue injury, depending on disease stage. Neutrophil extracellular traps (NETs) further exacerbate disease activity by promoting complement activation and autoantigen exposure, forming an amplifying inflammatory loop. Lupus nephritis remains challenging to monitor using conventional complement biomarkers such as CH50, C3, and C4; the utility of anti-C1q, anti-ficolin, and anti-C1s antibodies, along with tissue-based markers such as renal C4d and C5b-9 deposits, as markers of disease activity and prognosis, is discussed.
View Article and Find Full Text PDFSemin Arthritis Rheum
August 2025
Grupo IRIDIS (Investigation in Rheumatology and Immune-Diseases), Instituto de Investigación Sanitaria Galicia Sur, (IISGS), Hospital Universitario Vigo, Vigo, Spain.
Introduction: Systemic lupus erythematosus (SLE) is a heterogeneous autoimmune disorder characterized by multi-organ involvement and variable clinical manifestations. Recurrent clinical patterns suggest distinct phenotypes, where cluster analysis of autoantibodies could identify prognostic subtypes.
Objectives: To define and describe serological clusters and their clinical-epidemiological characteristics, as well as their association with comorbidities, disease activity measures, severity, and damage.
Lupus
September 2025
Department of Pharmacy, The Second Hospital of Hebei Medical University, Shijiazhuang, China.
ObjectiveTo systematically compare the clinical effectiveness and safety of Belimumab, Rituximab and Voclosporin in the treatment of lupus nephritis based on network meta-analysis method.MethodsSystematic search of registered clinical trials in four major databases (Pubmed, Embase, Web of Science, The Cochrane Register of Clinical Trials) and ClinicalTrials.gov.
View Article and Find Full Text PDFSci Adv
September 2025
Department of Medicine, Altman Clinical and Translational Research Institute, University of California, San Diego, La Jolla, CA 92093, USA.
Protein tyrosine phosphatase nonreceptor type 22 (PTPN22) is encoded by a gene strongly associated with lupus and other autoimmune diseases. PTPN22 regulates T cell receptor (TCR) signaling through dephosphorylation of the kinases lymphocyte-specific protein tyrosine kinase (LCK) and zeta-chain-associated protein kinase 70 (ZAP70). The regulation of PTPN22 remains poorly understood.
View Article and Find Full Text PDFInt Immunol
September 2025
Division of Innate Immunity, Department of Microbiology and Immunology, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Toll-like receptor 7 (TLR7) is an endosomal sensor that responds to both pathogen-derived and self-derived single-stranded RNA (ssRNA). Responses of TLR7 to self-derived ssRNA have been implicated in the development of autoimmune diseases, such as systemic lupus erythematosus (SLE). TLR7 antagonists and inhibitory anti-TLR7 monoclonal antibodies (mAbs) can protect lupus-prone NZBWF1 mice from lethal nephritis.
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