Autoantibodies and immune complexes

Autoantibodies are immunoglobulins produced by the immune system that inappropriately target the body's own tissues and proteins (StatPearls, 2023). Immune complexes are formed when these autoantibodies bind to their respective antigens, creating molecular aggregates that can circulate or deposit in various organs (Nature Reviews Rheumatology, 2021). These entities play a central role in the pathogenesis of Type II and Type III hypersensitivity reactions, driving inflammation through the activation of the complement system and recruitment of inflammatory cells via Fc receptors (NIH, 2022). In diseases like systemic lupus erythematosus and rheumatoid arthritis, the persistence of these complexes leads to chronic tissue damage in the kidneys, joints, and vasculature. Therapeutic interventions aim to mitigate these effects by inhibiting the production of autoantibodies, neutralizing their activity, or accelerating their removal from circulation. For instance, B-cell depleting therapies like rituximab reduce the source of new antibodies, while neonatal Fc receptor (FcRn) inhibitors like efgartigimod promote the rapid degradation of existing IgG (NEJM, 2021). Additionally, physical removal through plasmapheresis or immunoadsorption is utilized in acute, life-threatening manifestations of autoimmune disease to rapidly lower the burden of circulating pathogenic complexes.

Other names

Self-antibodiesCirculating immune complexesAntigen-antibody complexesPathogenic immunoglobulins

Therapeutic strategies involve the depletion of antibody-producing B cells, inhibition of neonatal Fc receptor (FcRn) to accelerate IgG degradation, physical removal via plasmapheresis or immunoadsorption, and neutralization of effector functions using high-dose IVIG (StatPearls, 2023; NEJM, 2021).