Macrophage scavenger receptor 1 (CD204) (CD204)

Macrophage scavenger receptor 1 (MSR1), also known as CD204 or Scavenger Receptor class A (SR-A), is a trimeric integral membrane glycoprotein primarily expressed on macrophages and dendritic cells (UniProt P21757). It functions as a pattern recognition receptor with broad ligand specificity, binding modified low-density lipoproteins (LDL), bacterial surface components, and apoptotic cells (NCBI Gene 4481). In the context of disease, CD204 plays a critical role in the development of atherosclerosis by mediating the formation of foam cells and is a key marker for pro-tumor M2-like tumor-associated macrophages (TAMs) (Frontiers in Immunology, 2022). High expression of CD204 in the tumor microenvironment is frequently associated with poor clinical prognosis across various cancers, including breast, lung, and ovarian cancer (Cancer Science, 2017). Therapeutic strategies targeting CD204 include the use of monoclonal antibodies to inhibit its immunosuppressive functions, small molecules like berberine to modulate inflammatory responses, and nanoparticles for targeted imaging and drug delivery (Frontiers in Immunology, 2022). However, therapeutic intervention must balance its role in host defense, as MSR1 is essential for the clearance of pathogens and the maintenance of tissue homeostasis (NCBI Gene 4481). Additionally, MSR1 has been implicated in the clearance of amyloid-beta in Alzheimer's disease, suggesting that its activation could be beneficial in neurodegenerative contexts (International Journal of Molecular Sciences, 2024). Overall, CD204 represents a versatile therapeutic target with significant implications in oncology, cardiology, and immunology.

Other names

MSR1Scavenger receptor class A member 1SCARA1SR-ASRAMacrophage scavenger receptor types I and IIMacrophage acetylated LDL receptor I and IIphSR1phSR2

Inhibition of modified LDL uptake to prevent foam cell formation, modulation of macrophage polarization from M2 to M1 phenotype to enhance anti-tumor immunity, blocking of negative regulatory signals to improve dendritic cell-mediated T cell activation, and activation of phagocytic pathways for the clearance of amyloid-beta plaques.