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Autoantibodies and soluble antigens are the primary constituents of immune complexes (ICs), which play a central role in the pathophysiology of various systemic autoimmune and inflammatory diseases. Autoantibodies are self-reactive immunoglobulins that bind to circulating or tissue-bound soluble antigens (autoantigens), forming aggregates that can deposit in vital organs such as the kidneys, joints, and blood vessels. These deposits trigger a cascade of inflammatory events, including the activation of the complement system and the engagement of Fc receptors on immune cells, leading to chronic tissue damage and organ dysfunction. Therapeutic strategies targeting these entities focus on reducing the overall burden of pathogenic complexes by inhibiting autoantibody production (e.g., B-cell depletion), accelerating their clearance (e.g., FcRn blockade), or physically removing them from the plasma (e.g., plasmapheresis). Monitoring the levels of specific autoantibodies and circulating immune complexes is a standard clinical practice for diagnosing autoimmune conditions and assessing the efficacy of immunomodulatory treatments.
Reduction of pathogenic autoantibody levels through neonatal Fc receptor (FcRn) inhibition, depletion of antibody-producing B-cells, or physical removal via extracorporeal circulation; neutralization of soluble antigens; and blockade of downstream inflammatory signaling pathways triggered by immune complexes.
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