Autoantibodies and autoreactive immune complexes

Autoantibodies are immunoglobulins produced by the immune system that inappropriately target and bind to the host's own proteins, cells, or tissues (Source: StatPearls, 2023). When these autoantibodies bind to their respective self-antigens, they form autoreactive immune complexes, which can deposit in tissues or circulate in the bloodstream, triggering inflammatory cascades (Source: Nature Reviews Rheumatology, 2018). The deposition of these complexes in tissues such as the renal glomeruli or neuromuscular junctions leads to localized inflammation and functional impairment (Source: JCI, 2020). These entities are primary drivers of pathology in numerous autoimmune diseases, including systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), and myasthenia gravis (MG), by inducing inflammation, activating the complement cascade, and promoting tissue destruction via leukocyte recruitment (Source: NIH, 2022). Therapeutic intervention often focuses on reducing the concentration of these pathogenic molecules through B-cell depletion, plasma exchange, or the use of neonatal Fc receptor (FcRn) antagonists, such as efgartigimod, which accelerate the degradation of IgG-type autoantibodies (Source: FDA, 2021). Monitoring the levels of specific autoantibodies and immune complexes serves as a critical diagnostic and prognostic tool in clinical practice (Source: Mayo Clinic, 2023).

Other names

Self-antibodiesPathogenic autoantibodiesCirculating immune complexesAutoreactive antibodiesPathogenic IgG

Therapeutic strategies include the use of neonatal Fc receptor (FcRn) antagonists to accelerate the catabolism of pathogenic IgG autoantibodies (Source: FDA, 2021), B-cell depletion therapy to inhibit the production of new autoantibodies (Source: StatPearls, 2023), physical removal of antibodies and complexes via therapeutic apheresis (Source: ASFA, 2019), and inhibition of the complement cascade triggered by immune complex deposition (Source: FDA, 2011).