Pathogenic autoantibodies and immune complexes (Autoantibodies/ICs)

Pathogenic autoantibodies are immunoglobulins produced by a dysregulated immune system that mistakenly target and bind to the body's own proteins, cells, or tissues. When these antibodies encounter their target self-antigens, they often form immune complexes—multimeric structures consisting of antibodies and antigens—that can circulate in the bloodstream or deposit directly into tissues such as the renal glomeruli, joints, and blood vessel walls. The deposition of these complexes triggers a potent inflammatory response, primarily through the activation of the classical complement pathway and the recruitment of inflammatory cells via Fc-gamma receptors, leading to chronic tissue damage and organ failure. In many autoimmune conditions, the concentration of these circulating pathogenic factors correlates directly with disease activity and severity. Modern therapeutic interventions, such as FcRn inhibitors, specifically aim to lower the half-life of these pathogenic IgG molecules, while other modalities like plasmapheresis or B-cell depletion focus on their physical removal or the cessation of their production, respectively.

Other names

Self-antibodiesCirculating immune complexesCICsPathogenic IgGAntinuclear antibodiesAuto-antibodies

Therapeutic strategies target these entities by accelerating their degradation through neonatal Fc receptor (FcRn) inhibition, physically removing them via plasma exchange, neutralizing them with high-dose IVIG, or preventing their formation by depleting B-cell populations.