An update on autoantibodies in systemic lupus erythematosus

Abstract

Purpose of reviewAutoantibodies are cornerstone biomarkers in systemic lupus erythematosus (SLE), an autoimmune disease characterized by autoantibody-mediated tissue damage. Autoantibodies can inform about disease susceptibility, clinical course, outcomes and the cause of SLE. Identifying pathogenic autoantibodies in SLE, however, remains a significant challenge. This review summarizes recent advances in the field of autoantibodies in SLE.Recent findingsHigh-throughput technologies and innovative hypothesis have been applied to identify autoantibodies linked to pathogenic pathways in SLE. This work has led to the discovery of functional autoantibodies targeting key components is SLE pathogenesis (e.g. DNase1L3, cytokines, extracellular immunoregulatory receptors), as well as the identification of endogenous retroelements and interferon-induced proteins as sources of autoantigens in SLE. Others have reinvigorated the study of mitochondria, which has antigenic parallels with bacteria, as a trigger of autoantibodies in SLE, and identified faecal IgA to nuclear antigens as potential biomarkers linking gut permeability and microbial translocation in SLE pathogenesis. Recent studies showed that levels of autoantibodies against dsDNA, C1q, chromatin, Sm and ribosomal P may serve as biomarkers of proliferative lupus nephritis, and identified novel autoantibodies to several unique species of Ro52 overexpressed by SLE neutrophils.SummaryAutoantibodies hold promise as biomarkers of pathogenic mechanisms in SLE.

Lupus Nephritis Risk Factors and Biomarkers: An Update

“…In contrast to other autoimmune kidney diseases that are restricted to a specific autoAb (e.g., anti-collagen IV Abs in glomerular basement membrane), a vast array of autoAbs characterize LN patients with distinct subsets present in the kidney [58]. Indeed, the pioneering experiment conducted by Mannik et al from 23 post-mortem kidneys revealed the presence of a large panel of polyreactive Abs targeting dsDNA/chromatin/histone, Sm/RNP, SSA/B, C1q, and phospholipids [59].…”

Interplay between the Chaperone System and Gut Microbiota Dysbiosis in Systemic Lupus Erythematosus Pathogenesis: Is Molecular Mimicry the Missing Link between Those Two Factors?

“…Autoantibodies circulating in body fluids or forming immune complexes in peripheral tissues have been used as valuable diagnostic and prognostic biomarkers in SLE for predicting pathogenic pathways and for guiding therapeutic treatments [ 123 , 124 ]. Therefore, in recent years, several efforts have been made to improve the detection of autoantibodies.…”

Anti-C1q antibodies: a biomarker for diagnosis and management of lupus nephritis. A narrative review

“…We think that in addition to anti-C1q, anti-dsDNA, anti-Smith (anti-Sm), anti-Ro/SSA, anti-La/SSB, anti-ribonucleoprotein (anti-RNP), anti-phospholipid antibodies, and complement fractions should be included in the panel of autoantibodies that any patients with suspected of LN should tested at baseline. Recently, anti-alfa enolase (ENO1), anti-histone 2 IgG2, antibodies directed against superoxide dismutase 2 (SOD2), anti-chromatin, anti-nucleosome and ribosomal P emerged in experimental studies, as possible biomarkers of active lupus nephritis, but are not yet available in the clinical setting ( 58 , 59 , 63 ). Considering the healthcare expenditure of testing the entire panel of available antibodies, complete screening should be performed at SLE diagnosis, while only anti-dsDNA, anti-C1q, and complement fractions should be tested to monitor LN during follow-up.…”