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Functional autoantibodies against G protein-coupled receptors (GPCR-AABs) are **endogenous IgG autoantibodies** that bind and allosterically modulate G protein-coupled receptors, a large family of membrane receptors involved in diverse signaling processes. Unlike classical autoantibodies that typically trigger inflammation or tissue destruction, GPCR-AABs can activate or inhibit receptor signaling in a persistent manner, disturbing physiological homeostasis. They are implicated in the pathogenesis or severity of various diseases, including autoimmune disorders, cardiovascular diseases, chronic inflammatory syndromes (such as Long COVID), and some neurological conditions. GPCR-AABs are increasingly recognized as *biomarkers* for certain diseases or for monitoring disease progression, rather than as direct therapeutic targets. As such, the **true molecular targets of clinical/drug intervention are the GPCRs themselves, not the autoantibodies**. Therefore, "G-protein coupled receptor functional autoantibody" is technically not a **therapeutic target** but rather a *disease-modifying agent or biomarker*, making the target designation incorrect.
Allosteric modulation of GPCR signaling. Pathological activation or inhibition of GPCR-mediated pathways. Disruption of receptor downregulation and desensitization mechanics.
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