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“Macrophage targets” refers to the diverse molecular and cellular structures on or within macrophages that have been proposed as points of therapeutic intervention. Macrophages are innate immune cells with critical roles in host defense, homeostasis, and disease pathogenesis. They display heterogeneous phenotypes (classically activated M1, alternatively activated M2 and subtypes) distinguished by surface markers and functional outputs. Targeting macrophages in disease settings (particularly cancer, chronic inflammation, and autoimmunity) includes strategies to deplete, reprogram, or inhibit their recruitment and signaling. However, the term “macrophage targets” is not a precise molecular entity but encompasses a wide range of surface receptors (e.g., mannose receptor CD206, Dectin-1, scavenger receptors, MerTK), intracellular pathways, and polarization states. Clinical strategies include monoclonal antibodies, small molecules, engineered cell therapies (e.g., CAR-Ms), and cytokine modulators, and the choice of “target” should be precisely defined at the molecular level for rational therapeutic design. For accurate and structured scientific or drug discovery purposes, the exact molecular target (such as “Mannose receptor (CD206)” or “Scavenger receptor class A (SR-A)”) must be specified rather than the umbrella term “macrophage targets”.
Depletion of macrophages (e.g., CSF1R inhibition); Reprogramming macrophage phenotype (e.g., promoting M1 over M2 polarization); Blocking recruitment to tumors (e.g., CCR2/CCR5 antagonists); Blocking checkpoint pathways (e.g., anti-CD47, anti-PD-1/PD-L1 therapies)
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