Macrophage M1 polarization

Macrophage M1 polarization refers to a cell state change, not a discrete molecule or receptor. It describes the switch of macrophages (a cell type in the innate immune system) into a "classically activated" M1 state, which is strongly pro-inflammatory, microbicidal, and involved in defense against pathogens[1][5]. M1 polarization is triggered by stimuli such as interferon-gamma (IFN-γ), lipopolysaccharide (LPS), and GM-CSF, which activate signaling cascades including the JAK/STAT, NF-κB, and MAPK pathways via receptors like IFNγR and TLR4[3][4][8]. M1-polarized macrophages produce high amounts of pro-inflammatory cytokines (TNFα, IL-12, IL-1β), reactive oxygen and nitrogen species, and upregulate antigen presentation, orchestrating immune and inflammatory responses[5][7]. Chronic or dysregulated M1 polarization is implicated in diseases like rheumatoid arthritis, multiple sclerosis, atherosclerosis, and infections[6][7]. M1 polarization is a biologic process—not a single molecular therapeutic target, protein, or receptor. Note: "Macrophage M1 polarization" is not a canonical molecular target, gene, or protein; rather, it is a phenotypic state/process. It is not suitable as a canonical target name under standard molecular drug target nomenclature.

Other names

M1 macrophage polarizationM1/M2 macrophage polarizationMacrophage polarization (M1/M2)