Pathogenic autoantibodies and their immune complexes (None)

Pathogenic autoantibodies are self-reactive immunoglobulins that target host antigens, leading to tissue damage and chronic inflammation (StatPearls, 2023). These antibodies can act directly by blocking or stimulating cellular receptors, or indirectly by forming immune complexes that deposit in tissues and trigger the classical complement pathway (Nature Reviews Rheumatology, 2021). Such processes are central to the pathogenesis of various autoimmune disorders, including systemic lupus erythematosus and myasthenia gravis (PubMed, PMID: 32814556). Therapeutic strategies focus on reducing the concentration of these pathogenic molecules through mechanisms such as neonatal Fc receptor (FcRn) inhibition, which accelerates the degradation of IgG (FDA, Vyvgart Label). Additionally, physical removal via plasmapheresis or the depletion of B cells to halt production are common clinical approaches (Journal of Clinical Apheresis, 2023). Monitoring specific autoantibody titers and complement levels is essential for diagnosing these conditions and evaluating the efficacy of targeted therapies (NIH, 2024).

Other names

Self-reactive antibodiesAuto-antibodiesCirculating immune complexesPathogenic IgGCIC

Neonatal Fc receptor (FcRn) antagonism to increase IgG catabolism; physical removal via therapeutic plasma exchange or immunoadsorption; B-cell depletion to reduce production; and neutralization by intravenous immunoglobulin (IVIG).