Abstract
The explosion of new information in recent years on the origin of macrophages in the steady-state and in the context of inflammation has opened up numerous new avenues of investigation and possibilities for therapeutic intervention. In contrast to the classical model of macrophage development, it is clear that tissue-resident macrophages can develop from yolk sac-derived erythro-myeloid progenitors, fetal liver progenitors, and bone marrow-derived monocytes. Under both homeostatic conditions and in response to pathophysiological insult, the contribution of these distinct sources of macrophages varies significantly between tissues. Furthermore, while all of these populations of macrophages appear to be capable of adopting the polarized M1/M2 phenotypes, their respective contribution to inflammation, resolution of inflammation, and tissue repair remains poorly understood and is likely to be tissue- and disease-dependent. A better understanding of the ontology and polarization capacity of macrophages in homeostasis and disease will be essential for the development of novel therapies that target the inherent plasticity of macrophages in the treatment of acute and chronic inflammatory disease.
Highlights
The M1/M2 polarization of macrophages in inflammation and disease resolution has been described
Kupffer cells Brain are largely based on studies that do not distinguish between resident macrophage and infiltrating macrophage populations
Given the emergence of technologies that help to distinguish resident cells from infiltrating cells, it will be essential to re-visit the M1/M2 paradigm in the context of macrophage ontogeny to determine the extent of plasticity of individual populations of macrophages
Summary
The M1/M2 polarization of macrophages in inflammation and disease resolution has been described.
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