Emerging areas for therapeutic discovery in SLE

Abstract

Recent advances in the field of autoimmunity have identified numerous dysfunctional pathways in Systemic Lupus Erythematosus (SLE), including aberrant clearance of nucleic-acid-containing debris and immune complexes, excessive innate immune activation leading to overactive type I IFN signalling, and abnormal B and T cell activation. On the background of genetic polymorphisms that reset thresholds for immune responses, multiple immune cells contribute to inflammatory amplification circuits. Neutrophils activated by immune complexes are a rich source of immunogenic nucleic acids. Identification of new B subsets suggests several mechanisms for induction of autoantibody producing effector cells. Disordered T cell regulation involves both CD4 and CD8 cells. An imbalance in immunometabolism in immune cells amplifies autoimmunity and inflammation. These new advances in understanding of disease pathogenesis provide fertile ground for therapeutic development.

IgA anti-dsDNA antibodies: A neglected serological parameter in systemic lupus erythematosus

“…Such self-antigen may originate from neutrophil extracellular traps (NETs), chromatin and the gut. 7,8 Toll-like receptor signalling on B cells has also been implicated in the production of autoantibodies, 7 as well as other signalling molecules such as B lymphocyte stimulator (BLyS) which is correlated with higher anti-dsDNA across all isotypes. 9 Anti-dsDNA can be of any isotype, although the IgG isoform is the most clinically relevant and best studied.…”

Colorimetry‐Based Phosphate Measurement for Polymerase Elongation

“…Extensive efforts have been made to identify variants in genomes. Highthroughput sequencing technology has identified many sequence variations, resulting in pathological consequences [1][2][3][4]. Targeted sequencing strategies can also be applied, such as the single-base extension (SBE) strategy.…”

Anti-C1q antibodies as a specific serological marker In patients with active lupus nephritis

“…Autoantibodies, immunological complexes, complement stimulation, and tissue inflammations are all produced due to immunological dysfunction, which results in clinical conditions with multi-organ affection and unexpected outcomes 2 . SLE affects several systemic organs, such as the musculoskeletal, mucocutaneous, cardiovascular, renal, and hematological systems 3 . Exacerbations or flares of SLE may vary in intensity from minor episodes that may be treated in the clinics to major episodes that require hospitalization.…”