M1/M2 macrophage polarization
DEM1/M2-Makrophagenpolarisierung
Reviewed by Maurice Lichtenberg
The M1/M2 framework describes macrophage activation states at two functional extremes: M1 (classically activated) macrophages, induced by IFN-γ and LPS, produce pro-inflammatory mediators including TNF-α, IL-6, IL-12, and reactive oxygen species; M2 (alternatively activated) macrophages, induced principally by IL-4 and IL-13 (and deactivated/suppressed by IL-10), promote tissue repair, phagocytosis of debris, and anti-inflammatory resolution. It is important to note that this binary model is a pedagogical simplification — current transcriptomic and proteomic data support a continuum of macrophage states that do not neatly map onto two poles. With aging, tissue macrophages tend toward a dysregulated inflammatory baseline, impairing resolution of acute inflammation and contributing to the chronic sterile inflammation underlying inflammaging.
Sources
- Gordon S, Taylor PR. (2005). Macrophage Polarization Comes of Age. *Immunity*doi:10.1016/j.immuni.2005.09.016
- Mahbub S, Deburghgraeve CR, Kovacs EJ. (2012). Advanced Age Impairs Macrophage Polarization. *Journal of Interferon & Cytokine Research*doi:10.1089/jir.2011.0058
