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Phospholipase A2 receptor (PLA2R) is a type I transmembrane glycoprotein that functions as a receptor for secretory phospholipase A2 (sPLA2s) and is a member of the C-type lectin receptor family, specifically related to the mannose receptor subgroup[1][6]. It is predominantly expressed on glomerular podocytes in the kidney and plays a regulatory role in podocyte biology and clearance of sPLA2s[6]. PLA2R serves as the major autoantigen in idiopathic membranous nephropathy, an autoimmune kidney disorder in which autoantibodies (anti-PLA2R antibodies) target key epitopes on the extracellular cysteine-rich domain of PLA2R, leading to immune complex formation, complement activation, and resultant glomerular damage[1][4][7]. Anti-PLA2R antibody levels are highly specific for primary membranous nephropathy, making this antibody both a diagnostic and prognostic biomarker; changes in antibody titer often precede clinical changes in disease activity and may guide therapy and risk assessment[2][5][6]. PLA2R itself is not directly targeted by current drugs, but immunosuppressive therapies indirectly decrease the pathogenic anti-PLA2R antibodies[5]. Note: The queried target, “anti-phospholipase A2 receptor antibody,” is an autoantibody (disease biomarker), not a molecular receptor or therapeutic target in the classical sense. The canonical therapeutic or molecular target is phospholipase A2 receptor (PLA2R), with the anti-PLA2R antibody being a clinically important biomarker for disease diagnosis and monitoring[5][6]. Thus, this entry contains a conceptual mix-up and has been annotated as is_incorrect: true.
Not directly targeted by drugs; disease-modifying agents suppress autoimmune response, thereby reducing anti-PLA2R antibody levels
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