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Innate immune scavenger and complement receptors represent a broad and diverse group of cell-surface proteins essential for the recognition and elimination of pathogens and cellular debris. Scavenger receptors (SRs), such as CD36 and Macrophage scavenger receptor 1 (MSR1), are pattern recognition receptors that bind a wide array of ligands, including modified lipoproteins and microbial components, facilitating phagocytosis and modulating inflammatory responses (PrabhuDas et al., 2017, J. Immunol.). Complement receptors (CRs), including Complement receptor 1 (CR1), Complement receptor 3 (CR3), and the C5a receptor (C5aR1), interact with fragments of the complement system to promote opsonization, chemotaxis, and the bridge between innate and adaptive immunity (Ricklin et al., 2010, Nat. Immunol.). These receptors are critically involved in the pathogenesis of various conditions, including atherosclerosis, where scavenger receptors contribute to foam cell formation, and chronic inflammatory diseases driven by complement dysregulation. Therapeutic interventions targeting these pathways include complement inhibitors like eculizumab and avacopan, which are used to treat paroxysmal nocturnal hemoglobinuria and ANCA-associated vasculitis, respectively (StatPearls, 2023). However, targeting these receptors carries risks, such as increased susceptibility to encapsulated bacterial infections due to impaired immune surveillance (PubMed, 2021).
Inhibition of complement cascade components or blockade of receptor-ligand interactions to modulate inflammatory signaling and phagocytic activity.
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