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Journal of Immunology Research
Volume 2018, Article ID 8917804, 25 pages
Review Article

Macrophage Polarization in Chronic Inflammatory Diseases: Killers or Builders?

1Department of Biomedical, Surgical and Dental Sciences, University of Milan, Milan, Italy
2Immunology and General Pathology Laboratory, Department of Biotechnology and Life Sciences, University of Insubria, Varese, Italy
3Scientific and Technologic Park, IRCCS MultiMedica, Milan, Italy

Correspondence should be addressed to Luca Parisi; ti.iminu@isirap.acul and Barbara Bassani; moc.liamg@ssab.eibab

Received 23 July 2017; Revised 1 November 2017; Accepted 15 November 2017; Published 14 January 2018

Academic Editor: Kebin Hu

Copyright © 2018 Luca Parisi et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Macrophages are key cellular components of the innate immunity, acting as the main player in the first-line defence against the pathogens and modulating homeostatic and inflammatory responses. Plasticity is a major feature of macrophages resulting in extreme heterogeneity both in normal and in pathological conditions. Macrophages are not homogenous, and they are generally categorized into two broad but distinct subsets as either classically activated (M1) or alternatively activated (M2). However, macrophages represent a continuum of highly plastic effector cells, resembling a spectrum of diverse phenotype states. Induction of specific macrophage functions is closely related to the surrounding environment that acts as a relevant orchestrator of macrophage functions. This phenomenon, termed polarization, results from cell/cell, cell/molecule interaction, governing macrophage functionality within the hosting tissues. Here, we summarized relevant cellular and molecular mechanisms driving macrophage polarization in “distant” pathological conditions, such as cancer, type 2 diabetes, atherosclerosis, and periodontitis that share macrophage-driven inflammation as a key feature, playing their dual role as killers (M1-like) and/or builders (M2-like). We also dissect the physio/pathological consequences related to macrophage polarization within selected chronic inflammatory diseases, placing polarized macrophages as a relevant hallmark, putative biomarkers, and possible target for prevention/therapy.