TABLE 1.
Representative studies reporting the ROS-promoted M2 polarization of macrophages.
| Model | Tested markers | ROS modulation | Mechanisms of M2 polarization | References |
|---|---|---|---|---|
| Mouse bone marrow-derived macrophages | M1: CD86, TNF-α, IL-12; M2: IL-10, CCL17/18/24 | O2 •− increment by NOX; elimination by BHA | ROS induce late-phase activation of ERK signaling | Zhang, et al. (2013) |
| Mouse RAW 264.7 macrophages | M1: CD11b; M2: CD206, Arg-1 | mtROS; reduction by antioxidant | Antioxidant reduce M2 type via ROS/ERK and mTOR pathway | Shan, et al. (2017) |
| Primary human macrophages | M1: TNF-α, IL12b; M2: CD163, CD206 | Increased via H2O2 addition; reduced using MnTe | Presumably induce Stat3 activation for M2 polarization | Griess, et al. (2020) |
| Monocytes in human peripheral blood mononuclear cells | M1: not tested; M2: CD163, CD206 | Increment via CAF stimulation; reduction by BHA | Not directly tested | Zhang, et al. (2017) |
| Mouse bone marrow-derived macrophages | M1: IL-6; M2: Arg-1, Mrc1, IL-10, Ym2, Fizz1 | mtROS increment via GMFG knockdown; reduction by antioxidant | Increased mtROS presumably alters iron metabolism-related protein expression | Aerbajinai, et al. (2019) |
| Murine peritoneal macrophage | M1: IL-6, TNF-α, IL-1β; M2: Arg-1, Ym1, Fizz1-Relm-α | MCPIP-stimulated ROS production | ROS induced ER stress and autophagy to increase M2 markers | Kapoor, et al. (2015) |
NOX: NADPH, oxidase; Arg-1: arginase-1; mtROS: mitochondria ROS; mTOR: mammalian target of rapamycin; MnTe: MnTE-2-PyP5+; Stat3: signal transducer and activator of transcription 3; CAF: cancer-associated fibroblasts; GMFG: glia maturation factor-λ; MCPIP: MCP-1-induced protein.