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Autoantibodies and pathogenic antigens represent the molecular components responsible for the initiation and progression of autoimmune diseases (StatPearls, 2023). Autoantibodies are immunoglobulins produced by the host's immune system that mistakenly target self-proteins, referred to as pathogenic antigens or autoantigens (NIH, 2020). This binding triggers a cascade of inflammatory processes, including complement activation and recruitment of effector cells, leading to tissue damage and organ dysfunction (PubMed, 2021). These entities are central to the pathology of numerous conditions such as myasthenia gravis, systemic lupus erythematosus, and rheumatoid arthritis (Nature Reviews Rheumatology, 2020). Therapeutic approaches often focus on reducing the load of these pathogenic molecules by accelerating their clearance via neonatal Fc receptor (FcRn) inhibition or by depleting the B-cell populations that produce them (Nature Reviews Drug Discovery, 2022). Consequently, measuring the levels of specific autoantibodies is a cornerstone of clinical diagnosis and monitoring treatment efficacy in autoimmune disorders. Note: This entry describes a broad category of immune components rather than a single molecular target.
Therapeutic strategies targeting this axis include the reduction of circulating pathogenic IgG autoantibodies through neonatal Fc receptor (FcRn) antagonism, the depletion of B-lymphocytes to inhibit the production of new autoantibodies, and the neutralization of self-reactive antibodies using high-dose intravenous immunoglobulin (IVIG).
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