One cannot discuss anti-dsDNA antibodies and lupus nephritis without discussing the nature of Systemic lupus erythematosus (SLE). SLE is insistently described as a prototype autoimmune syndrome, with anti-dsDNA antibodies as a central biomarker and a pathogenic factor. The two entities, "SLE" and "The Anti-dsDNA Antibody," have been linked in previous and contemporary studies although serious criticism to this mutual linkage have been raised: Anti-dsDNA antibodies were first described in bacterial infections and not in SLE; later SLE, viral and parasitic infections and in malignancies. An increasing number of studies on classification criteria for SLE have been published in the aftermath of the canonical 1982 American College of Rheumatology SLE classification sets of criteria. Considering these studies, it is surprising to observe a nearby complete absence of fundamental critical/theoretical discussions aimed to explain how and why the classification criteria are linked in context of etiology, pathogenicity, or biology. This study is an attempt to prioritize critical comments on the contemporary definition and classification of SLE and of anti-dsDNA antibodies in context of lupus nephritis. Epidemiology, etiology, pathogenesis, and measures of therapy efficacy are implemented as problems in the present discussion. In order to understand whether or not disparate clinical SLE phenotypes are useful to determine its basic biological processes accounting for the syndrome is problematic. A central problem is discussed on whether the clinical role of anti-dsDNA antibodies from principal reasons can be accepted as a biomarker for SLE without clarifying what we define as an anti-dsDNA antibody, and in which biologic contexts the antibodies appear. In sum, this study is an attempt to bring to the forum critical comments on the contemporary definition and classification of SLE, lupus nephritis and anti-dsDNA antibodies. Four concise hypotheses are suggested for future science at the end of this analytical study.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7573073 | PMC |
http://dx.doi.org/10.3389/fimmu.2020.569234 | DOI Listing |
Int J Rheum Dis
January 2025
Department of Rheumatology and Immunology, The Drum Tower Clinical Medical School of Nanjing Medical University, Nanjing, Jiangsu, China.
Background: γδT cells have been implicated in the pathogenesis of autoimmune diseases. The study aims to investigate the abundance of γδT cells in MRL/lpr mice.
Methods: MRL/lpr mice were used as lupus models, while C3H/HeJ mice served as normal controls.
Autoimmunity
December 2025
Department of Clinical Immunology & Allergy, Westmead Hospital & ICPMR, Westmead, NSW, Australia.
Systemic lupus erythematosus (SLE) is an extremely heterogenous autoimmune disorder. A key biomarker, the double stranded (ds) DNA autoantibody, provides diagnostic specificity for SLE. We analyzed anti-dsDNA by mass spectrometry (MS) to determine if ascertaining the autoantibody's heavy chain variable region (IGHV) may hold any clinical relevance.
View Article and Find Full Text PDFAutoimmun Rev
December 2024
Reichman University, Herzelia, Israel; Zabludowicz Center for Autoimmune Diseases (Founder), Sheba Medical Center, Tel-Hashomer, Israel.
Background: Low vitamin D levels are commonly observed in autoimmune diseases, suggesting a potential role in disease pathogenesis. The presence of anti-vitamin D antibodies may contribute to these deficiencies and influence autoimmune processes.
Objective: To review and analyze studies investigating the occurrence of anti-vitamin D antibodies in autoimmune diseases.
Part Fibre Toxicol
December 2024
Louvain Centre for Toxicology and Applied Pharmacology (LTAP), Institute of Experimental and Clinical Research (IREC), Université catholique de Louvain (UCLouvain), Brussels, Belgium.
Scand J Immunol
January 2025
Division of Rheumatology, Department of Medicine, Karolinska Institutet, Karolinska University Hospital Solna, Stockholm, Sweden.
Altered composition of B-cell compartments is a known feature in patients with systemic lupus erythematosus (SLE). However, deep characterisation of B-cell subsets and their relation to clinical manifestations and disease activity in patients is limited. In this study, we analysed peripheral B-cell subsets phenotype in SLE (n = 35) and healthy controls (HCs, n = 15) by spectral flow cytometry.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!