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      Molecular Mechanisms That Influence the Macrophage M1–M2 Polarization Balance

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          Abstract

          As an essential component of innate immunity, macrophages have multiple functions in both inhibiting or promoting cell proliferation and tissue repair. Diversity and plasticity are hallmarks of macrophages. Classical M1 and alternative M2 activation of macrophages, mirroring the Th1–Th2 polarization of T cells, represent two extremes of a dynamic changing state of macrophage activation. M1-type macrophages release cytokines that inhibit the proliferation of surrounding cells and damage contiguous tissue, and M2-type macrophages release cytokines that promote the proliferation of contiguous cells and tissue repair. M1–M2 polarization of macrophage is a tightly controlled process entailing a set of signaling pathways, transcriptional and posttranscriptional regulatory networks. An imbalance of macrophage M1–M2 polarization is often associated with various diseases or inflammatory conditions. Therefore, identification of the molecules associated with the dynamic changes of macrophage polarization and understanding their interactions is crucial for elucidating the molecular basis of disease progression and designing novel macrophage-mediated therapeutic strategies.

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          Most cited references119

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          Exploring the full spectrum of macrophage activation.

          Macrophages display remarkable plasticity and can change their physiology in response to environmental cues. These changes can give rise to different populations of cells with distinct functions. In this Review we suggest a new grouping of macrophage populations based on three different homeostatic activities - host defence, wound healing and immune regulation. We propose that similarly to primary colours, these three basic macrophage populations can blend into various other 'shades' of activation. We characterize each population and provide examples of macrophages from specific disease states that have the characteristics of one or more of these populations.
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            Macrophage plasticity and polarization: in vivo veritas.

            Diversity and plasticity are hallmarks of cells of the monocyte-macrophage lineage. In response to IFNs, Toll-like receptor engagement, or IL-4/IL-13 signaling, macrophages undergo M1 (classical) or M2 (alternative) activation, which represent extremes of a continuum in a universe of activation states. Progress has now been made in defining the signaling pathways, transcriptional networks, and epigenetic mechanisms underlying M1-M2 or M2-like polarized activation. Functional skewing of mononuclear phagocytes occurs in vivo under physiological conditions (e.g., ontogenesis and pregnancy) and in pathology (allergic and chronic inflammation, tissue repair, infection, and cancer). However, in selected preclinical and clinical conditions, coexistence of cells in different activation states and unique or mixed phenotypes have been observed, a reflection of dynamic changes and complex tissue-derived signals. The identification of mechanisms and molecules associated with macrophage plasticity and polarized activation provides a basis for macrophage-centered diagnostic and therapeutic strategies.
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              Macrophage polarization: tumor-associated macrophages as a paradigm for polarized M2 mononuclear phagocytes.

              Mononuclear phagocytes are versatile cells that can express different functional programs in response to microenvironmental signals. Fully polarized M1 and M2 (or alternatively activated) macrophages are the extremes of a continuum of functional states. Macrophages that infiltrate tumor tissues are driven by tumor-derived and T cell-derived cytokines to acquire a polarized M2 phenotype. These functionally polarized cells, and similarly oriented or immature dendritic cells present in tumors, have a key role in subversion of adaptive immunity and in inflammatory circuits that promote tumor growth and progression.
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                Author and article information

                Contributors
                Journal
                Front Immunol
                Front Immunol
                Front. Immunol.
                Frontiers in Immunology
                Frontiers Media S.A.
                1664-3224
                28 November 2014
                2014
                : 5
                : 614
                Affiliations
                [1] 1State Key Laboratory of Pharmaceutical Biotechnology, Nanjing University School of Life Sciences , Nanjing, China
                [2] 2Jiangsu Engineering Research Center for MicroRNA Biology and Biotechnology (JERC-MBB), Nanjing University School of Life Sciences , Nanjing, China
                Author notes

                Edited by: Laurel L. Lenz, University of Colorado School of Medicine, USA

                Reviewed by: John P. Vasilakos, 3M Company, USA; Charles Dudley Mills, BioMedical Consultants, USA

                *Correspondence: Ke Zen, State Key Laboratory of Pharmaceutical Biotechnology, Jiangsu Engineering Research Center for MicroRNA Biology and Biotechnology (JERC-MBB), Room A229, School of Life Sciences, Xianlin Campus of Nanjing University, No. 163, Xianlin Road, Qixia District, Nanjing, Jiangsu 210046, China e-mail: kzen@ 123456nju.edu.cn

                This article was submitted to Molecular Innate Immunity, a section of the journal Frontiers in Immunology.

                Article
                10.3389/fimmu.2014.00614
                4246889
                25506346
                b06d7750-69b8-47ab-a000-e14632783813
                Copyright © 2014 Wang, Liang and Zen.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                : 14 August 2014
                : 14 November 2014
                Page count
                Figures: 1, Tables: 0, Equations: 0, References: 116, Pages: 9, Words: 8548
                Categories
                Immunology
                Review Article

                Immunology
                innate immune response,macrophage polarization,tlr,nlr,socs,microrna
                Immunology
                innate immune response, macrophage polarization, tlr, nlr, socs, microrna

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