Reticuloendothelial system cell (macrophage) (RES cell or macrophage (commonly, "RES" for the system, "MΦ" for macrophages, but no universal standard—most scientific texts use "macrophage"))

The **reticuloendothelial system (RES)**, now often termed the **mononuclear phagocyte system (MPS)**, comprises primarily macrophages and some specialized endothelial cells distributed throughout the body—in organs such as the liver (Kupffer cells), spleen, lymph nodes, and bone marrow[1][3][5][7][9]. **Macrophages** are derived from blood monocytes and serve as phagocytes that engulf pathogens, dead cells, and foreign material. They participate in immune defense, tissue homeostasis, iron recycling, and inflammation. While RES/macrophages as a cell type are essential for defense and tissue repair, they also represent a major barrier for nanoparticle drug delivery, as they rapidly clear such particles from circulation[8]. In disease, macrophages can contribute to chronic inflammation, tissue damage, tumor progression, and atherosclerosis, depending on activation status and localization[4][5]. "Reticuloendothelial system cells/macrophages" is not a molecularly defined drug target, but specific surface proteins or signaling molecules on these cells are emerging as important therapeutic targets. If you need structured target information for a **molecularly defined marker** or receptor on macrophages (such as "CD36", "CCR2", or "scavenger receptor"), a new, more specific entry is necessary.

Other names

Mononuclear phagocyte system cellRES cellPhagocytic cell (of RES)Histiocyte (sometimes used for tissue macrophages)Scavenger cell

Inhibition of phagocytosis or endocytosis (e.g., SIRPα/CD47 blockade) Depletion or modulation of macrophage activity (via nanoparticle overloading or antibody targeting) Inhibition of recruitment/migration (e.g., CCR2 blockade) Modulation of cytokine release or immune response