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Pathogenic autoantibodies are abnormal immunoglobulins produced by the adaptive immune system that mistakenly recognize self-molecules as foreign. When these bind their targets, they can directly disrupt physiological processes—by blocking receptors, mimicking ligands/receptor stimulation—or trigger destructive inflammatory cascades through complement fixation and recruitment/activation of leukocytes such as neutrophils. Immune complexes form when antibodies bind soluble antigens; if not efficiently cleared, they deposit in tissues where they activate complement and recruit inflammatory cells leading to local damage—a hallmark mechanism in many autoimmune diseases such as systemic lupus erythematosus and vasculitis syndromes. Both pathogenic autoantibodies and immune complexes represent key drivers—and therapeutic targets—in a range of autoimmune conditions characterized by chronic inflammation and organ dysfunction resulting from inappropriate humoral immunity.[1][3][5][6]
Drugs act via several mechanisms depending on the context, including: - Physical removal from circulation via plasma exchange/plasmapheresis[4] - Suppression or depletion of antibody-producing B cells - Inhibition of complement activation to prevent tissue damage mediated by antibody/complex deposition[1]
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