Macrophage Polarization in Bacterial Infections

By M. Benoit, B. Desnues, J. Mege. Journal of Immunology, 2008

1,309 citations recorded by the source corpus.

Subfields: Immunology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/3d48808ddbf256f5554c0e1cf21e911de15964f2

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Citations in the corpus

Understanding the Mysterious M2 Macrophage through Activation Markers and Effector Mechanisms (2015, background): “This review discusses whether theseM2markers can be reliably used to identifyM2macrophages and define their functional subdivisions.”
Multifunctional Coatings to Simultaneously Promote Osseointegration and Prevent Infection of Orthopaedic Implants (2016, neutral): “[143] Once at the infection site, the macrophages start their own signaling cascade, in combination with bone marrow stromal cells, which eventually leads to differentiation into osteoclasts and hence lo al bone resorption.”
The Pathogenesis of Sepsis (2011, background): “Macrophages phagocytose bacteria and produce a range of proinflammatory cytokines, which initiate the innate immune system’s response to the bacterial pathogen (2).”
Krüppel-like factor 4 regulates macrophage polarization. (2011, background): “Furthermore, ex vivo studies confirmed that migration of KLF4-deficient macrophages in response to the prototypical monocyte/macrophage chemokine MCP-1 was similar to that of control cells (Supplemental Figure 11B).”
Macrophage Dysfunction Impairs Resolution of Inflammation in the Wounds of Diabetic Mice (2010, background): “Since the introduction of the concept of alternative activation of macrophages in 1992 [63], these cells have been broadly assigned to two broad groups: (i) classically activated or type I macrophages (M1) which are pro-inflammatory effectors, and (ii) alternatively activated or type II macrophages ”
Macrophage plasticity, polarization, and function in health and disease (2018, background): “…like aMycobacterium tuberculosis (MTB) might suppress macrophage to avoid cytotoxic functions and evade the cellular immune response or repolarize M1 polarized macrophages toward an M2 phenotype (Bai et al., 2013; Benoit et al., 2008; Kaufmann, 2016; Mege et al., 2011; Murray & Wynn, 2011b).”
The Jmjd3-Irf4 axis regulates M2 macrophage polarization and host responses against helminth infection (2010, background): “M1 macrophages produce large amounts of nitric oxide by expressing inducible nitric oxide synthase (iNOS) and tumor necrosis factor (TNF), and are essential for clearing bacterial, viral and fungal infection”
Macrophages in Tumor Microenvironments and the Progression of Tumors (2012, background): “For example, the IL-12 produced by M1 macrophages can promote the differentiation of Th1 cells, which can improve antigen phagocytosis [12, 16].”
IL-33 Amplifies the Polarization of Alternatively Activated Macrophages That Contribute to Airway Inflammation1 (2009, background): “M2 macrophages, in contrast, are characterized by their low secretion of IL-12 and can be further subdivided into three groups: M2a (alternatively activated macrophages, AAM(3)), induced by IL-4 or IL-13 or IL-21; M2b, induced by immune complexes and agonists of TLRs or IL-1 receptors; and M2c (immu”
Metabolic Pathways In Immune Cell Activation And Quiescence (2013, background): “Interferon g (IFN-g), in combination with TLR agonists, promotes M1 (or classical) activation, whereas the cytokines IL-4 and IL-13 promoteM2 (or alternative) activation (Benoit et al., 2008; Gordon, 2003; Murray and Wynn, 2011).”
Overview of the Immune Response (2003, background): “Depending on the nature of activating signals that are present when macrophages differentiate from immature precursor cells and when they receive their first activation signal, macrophages can adopt one of several phenotypes.(12) Classically activated macrophages produce large amounts of IFN-g, IL-6”
Novel Markers to Delineate Murine M1 and M2 Macrophages (2015, methodology): “Release of pathogen or danger-associated molecular patterns (PAMPs or DAMPs) and IFN-γ during infection or tissue injury promotes classical macrophage activation and ensures tissue sterility [5].”
Microglial M1/M2 polarization and metabolic states (2016, background): “Activation of the PPAR-γ characterizes M2 polarization (Benoit et al., 2008a; Rajaram et al., 2010).”