Circulating pathogenic autoantibodies

Circulating pathogenic autoantibodies are immunoglobulins produced by the immune system that mistakenly target and react with the body's own tissues, cells, or soluble factors (Ludwig et al., 2017, Frontiers in Immunology) [1]. These molecules play a central role in the pathogenesis of numerous autoimmune disorders by inducing inflammation, activating the complement cascade, or interfering with normal cellular signaling, such as blocking receptors at the neuromuscular junction (El-Haidari et al., 2021, Nature Reviews Rheumatology) [2]. In clinical practice, they serve as both diagnostic markers and direct therapeutic targets for intervention [1]. Modern pharmacological strategies to address these autoantibodies include inhibiting the neonatal Fc receptor (FcRn) to accelerate their degradation, depleting B-cells to prevent their synthesis, or physically removing them from the blood through therapeutic apheresis (FDA, 2021; Padmanabhan et al., 2019) [3, 4]. Reducing the concentration of these pathogenic proteins is a primary goal in managing acute exacerbations and chronic symptoms of antibody-mediated diseases [2].

Other names

AutoantibodiesSelf-reactive antibodiesPathogenic immunoglobulinsHumoral autoantibodies

Reduction of circulating autoantibody levels through accelerated degradation via FcRn inhibition, physical removal via therapeutic plasma exchange, or suppression of production via B-cell depletion and plasma cell inhibition.