Macrophage Polarization in Chronic Inflammatory Diseases: Killers or Builders?

Figure 4

Macrophage polarization in atherosclerosis. Macrophages are crucial players involved in the atherosclerosis development due to their ability to regulate cholesterol efflux. In this context, the upregulation of LXRs in M2 macrophages has been found to exert a protective role. Indeed, LRXs reduce peripheral tissue excess cholesterol that is returned to the liver by releasing HDL in the plasma (A). Apart from M1 and M2 polarization, a third macrophage state has been described in the atherosclerosis context that is termed Mox. Macrophages exposed to oxidized phospholipids display reduced phagocytic and chemotactic abilities compared with M1- and M2-like macrophages and are characterized by the expression of the transcription factor NFE2L2 as far as Hmox1, Srxn1, Txnrd1, and Gsr genes. Mox macrophages also activate TLR2­dependent mechanisms in response to oxidized lipids leading to an increase of IL­1β and COX-2 (B).