Macrophages are key orchestrators of chronic inflammation. They respond to microenvironmental signals with polarized genetic and functional programmes.   M1 macrophages which are classically activated by microbial products and interferon-γ, are potent effector cells which kill microorganisms and tumors. In contrast, M2 cells, tune inflammation and adaptive immunity; promote cell proliferation by producing growth factors and products of the arginase pathway (ornithine and polyamines); scavenge debris by expressing scavenger receptors; promote angiogenesis, tissue remodeling and repair. M1 and M2 cells represent simplified extremes of a continuum of functional states. Available information suggests that TAM are a prototypic M2 population.  M2 polarization of phagocytes sets these cells  in a tissue remodeling and repair mode and orchestrate the smouldering and polarized chronic inflammation associated to established neoplasia. Recent studies have begun to address the central issue of the relationship between genetic events causing cancer and activation of protumor, smoldering, non resolving tumor-promoting inflammation.  New vistas have emerged on molecules associated with M2 or M2-like polarization and its orchestration. Macrophage polarization has emerged as a key determinant of resolution of inflammation.

References

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