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      M2b macrophage polarization and its roles in diseases

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          Abstract

          Macrophages play an important role in a wide variety of physiologic and pathologic processes. Plasticity and functional polarization are hallmarks of macrophages. Macrophages commonly exist in two distinct subsets: classically activated macrophages (M1) and alternatively activated macrophages (M2). M2b, a subtype of M2 macrophages, has attracted increasing attention over the past decade due to its strong immune‐regulated and anti‐inflammatory effects. A wide variety of stimuli and multiple factors modulate M2b macrophage polarization in vitro and in vivo. M2b macrophages possess both protective and pathogenic roles in various diseases. Understanding the mechanisms of M2b macrophage activation and the modulation of their polarization might provide a great perspective for the design of novel therapeutic strategies. The purpose of this review is to discuss current knowledge of M2b macrophage polarization, the roles of M2b macrophages in a variety of diseases and the stimuli to modulate M2b macrophage polarization.

          Abstract

          Review outlines the current knowledge of the stimuli of M2b macrophage polarization and the roles of these cells in diseases.

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          Most cited references131

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          Macrophage plasticity, polarization, and function in health and disease.

          Macrophages are heterogeneous and their phenotype and functions are regulated by the surrounding micro-environment. Macrophages commonly exist in two distinct subsets: 1) Classically activated or M1 macrophages, which are pro-inflammatory and polarized by lipopolysaccharide (LPS) either alone or in association with Th1 cytokines such as IFN-γ, GM-CSF, and produce pro-inflammatory cytokines such as interleukin-1β (IL-1β), IL-6, IL-12, IL-23, and TNF-α; and 2) Alternatively activated or M2 macrophages, which are anti-inflammatory and immunoregulatory and polarized by Th2 cytokines such as IL-4 and IL-13 and produce anti-inflammatory cytokines such as IL-10 and TGF-β. M1 and M2 macrophages have different functions and transcriptional profiles. They have unique abilities by destroying pathogens or repair the inflammation-associated injury. It is known that M1/M2 macrophage balance polarization governs the fate of an organ in inflammation or injury. When the infection or inflammation is severe enough to affect an organ, macrophages first exhibit the M1 phenotype to release TNF-α, IL-1β, IL-12, and IL-23 against the stimulus. But, if M1 phase continues, it can cause tissue damage. Therefore, M2 macrophages secrete high amounts of IL-10 and TGF-β to suppress the inflammation, contribute to tissue repair, remodeling, vasculogenesis, and retain homeostasis. In this review, we first discuss the basic biology of macrophages including origin, differentiation and activation, tissue distribution, plasticity and polarization, migration, antigen presentation capacity, cytokine and chemokine production, metabolism, and involvement of microRNAs in macrophage polarization and function. Secondly, we discuss the protective and pathogenic role of the macrophage subsets in normal and pathological pregnancy, anti-microbial defense, anti-tumor immunity, metabolic disease and obesity, asthma and allergy, atherosclerosis, fibrosis, wound healing, and autoimmunity.
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            Understanding the Mysterious M2 Macrophage through Activation Markers and Effector Mechanisms

            The alternatively activated or M2 macrophages are immune cells with high phenotypic heterogeneity and are governing functions at the interface of immunity, tissue homeostasis, metabolism, and endocrine signaling. Today the M2 macrophages are identified based on the expression pattern of a set of M2 markers. These markers are transmembrane glycoproteins, scavenger receptors, enzymes, growth factors, hormones, cytokines, and cytokine receptors with diverse and often yet unexplored functions. This review discusses whether these M2 markers can be reliably used to identify M2 macrophages and define their functional subdivisions. Also, it provides an update on the novel signals of the tissue environment and the neuroendocrine system which shape the M2 activation. The possible evolutionary roots of the M2 macrophage functions are also discussed.
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              IRF5 promotes inflammatory macrophage polarization and TH1-TH17 responses.

              Polymorphisms in the gene encoding the transcription factor IRF5 that lead to higher mRNA expression are associated with many autoimmune diseases. Here we show that IRF5 expression in macrophages was reversibly induced by inflammatory stimuli and contributed to the plasticity of macrophage polarization. High expression of IRF5 was characteristic of M1 macrophages, in which it directly activated transcription of the genes encoding interleukin 12 subunit p40 (IL-12p40), IL-12p35 and IL-23p19 and repressed the gene encoding IL-10. Consequently, those macrophages set up the environment for a potent T helper type 1 (T(H)1)-T(H)17 response. Global gene expression analysis demonstrated that exogenous IRF5 upregulated or downregulated expression of established phenotypic markers of M1 or M2 macrophages, respectively. Our data suggest a critical role for IRF5 in M1 macrophage polarization and define a previously unknown function for IRF5 as a transcriptional repressor.
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                Author and article information

                Contributors
                gyguoyz@163.com
                Journal
                J Leukoc Biol
                J. Leukoc. Biol
                10.1002/(ISSN)1938-3673
                JLB
                Journal of Leukocyte Biology
                John Wiley and Sons Inc. (Hoboken )
                0741-5400
                1938-3673
                21 December 2018
                August 2019
                : 106
                : 2 , Special Focus Issue: Tissue Phagocyte Heterogeneity in Health and Disease (AAI/SLB) ( doiID: 10.1002/jlb.2019.106.issue-2 )
                : 345-358
                Affiliations
                [ 1 ] Guangdong Metabolic Disease Research Center of Integrated Chinese and Western Medicine Joint Laboratory of Guangdong Hong Kong and Macao on Glycolipid Metabolic Diseases Guangdong Key Laboratory of Metabolic Disease Prevention and Treatment of Traditional Chinese Medicine Institute of Chinese Medicine Sciences Guangdong Pharmaceutical University Guangzhou China
                Author notes
                [*] [* ] Correspondence

                Jiao Guo, Guangdong Pharmaceutical University, 280 Wai Huan Dong Road Guangzhou 510006, China.

                Email: gyguoyz@ 123456163.com

                Article
                JLB10302
                10.1002/JLB.3RU1018-378RR
                7379745
                30576000
                a989dee6-b46c-43c3-ab2d-72c7d091d1fd
                ©2018 The Authors. Society for Leukocyte Biology Published by Wiley Periodicals, Inc.

                This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

                History
                : 03 October 2018
                : 07 December 2018
                : 09 December 2018
                Page count
                Figures: 3, Tables: 1, Pages: 14, Words: 10715
                Funding
                Funded by: National Natural Science Foundation of China , open-funder-registry 10.13039/501100001809;
                Award ID: 81503313
                Award ID: 81530102
                Funded by: Natural Science Foundation of Guangdong Province , open-funder-registry 10.13039/501100003453;
                Award ID: 2018A030310403
                Funded by: Medical Scientific Research Foundation of Guangdong Province
                Award ID: A2018068 for
                Categories
                Review
                Reviews
                Custom metadata
                2.0
                August 2019
                Converter:WILEY_ML3GV2_TO_JATSPMC version:5.8.5 mode:remove_FC converted:24.07.2020

                Hematology
                autoimmunity,chemokines,disease pathogenesis,inflammation,manipulation of immune response,monocyte/macrophage

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