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Pathogens, autoantigens, and autoantibodies represent the complex tripartite interplay involved in the initiation and progression of autoimmune diseases (Smatti et al., 2019, Frontiers in Microbiology). Pathogens, such as viruses and bacteria, are frequently identified as environmental triggers that can initiate autoimmunity through mechanisms like molecular mimicry, where microbial antigens share structural similarities with host proteins (Cusick et al., 2012, Clinical Reviews in Allergy & Immunology). Autoantigens are the specific endogenous molecules, such as double-stranded DNA or myelin basic protein, that become the targets of a misdirected immune response. Autoantibodies are the immunoglobulins produced by B cells that bind to these autoantigens, serving as both diagnostic biomarkers and active mediators of tissue damage and inflammation (Ludwig et al., 2017, Frontiers in Immunology). This collective concept is fundamental to understanding the etiology of conditions like Systemic Lupus Erythematosus and Multiple Sclerosis, but it does not constitute a single druggable target. Instead, therapeutic strategies focus on specific components within this axis, such as B-cell depletion, cytokine inhibition, or the management of underlying infections.
Not applicable as this represents a broad category of biological entities rather than a single therapeutic target.
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