Macrophage activation and polarization.
By F. Martínez, A. Sica, A. Mantovani, M. Locati. Frontiers in Bioscience, 2008
3,225 citations recorded by the source corpus.
Subfields: Immunology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/00723db493012f2f431a3ce17741a5dda2dc1c6a
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Citations in the corpus
- TNF and increased intracellular iron alter macrophage polarization to a detrimental M1 phenotype in the injured spinal cord. (2014, neutral): “Interferon-g (IFN-g, the prototypic T helper 1 [Th1] cytokine) and the Toll-like receptor-4 (TLR-4) ligand, lipopolysaccharide (LPS), induce M1 polarization, while the Th2 cytokine IL-4 and other factors induce M2 polarization (David and Kroner, 2011; Gordon and Taylor, 2005).”
- International Union of Basic and Clinical Pharmacology. LXXXIX. Update on the Extended Family of Chemokine Receptors and Introducing a New Nomenclature for Atypical Chemokine Receptors (2014, neutral): “…macrophages have been demonstrated to be activated by the tumor microenvironment to an alternatively activated M2 phenotype, which supports tumor growth by different mechanisms, including promotion of angiogenesis and matrix remodeling and direct tumor cell growth (Martinez et al., 2008).”
- Phenotypic Switching of Adipose Tissue Macrophages With Obesity Is Generated by Spatiotemporal Differences in Macrophage Subtypes (2008, background): “However, under the influence of TH2 cytokines interleukin (IL)-4 or IL-13, macrophages assume an alternative activation state (M2a) and produce immunosuppressive factors, such as IL-10, IL-1RA, and arginase (9).”
- Microglial M1/M2 polarization and metabolic states (2016, background): “M2c polarization occurs in response to specific anti-inflammatory factors such as, IL-10, TGF-β and glucocorticoids (Vodovoz et al., 1993; Gordon, 2003; Martinez et al., 2008; Morris, 2009; Mills, 2012).”
- Immune-responsive gene 1 protein links metabolism to immunity by catalyzing itaconic acid production (2013, background): “Appl Microbiol Biotechnol 80(2):223–229.”
- Mesenchymal stem cell-macrophage crosstalk and bone healing (2018, background): “inflammatory macrophages are called classically activated or M1 macrophages, while macrophages active in tissue regeneration are known as alternatively activated or M2 macrophages [21].”
- Nitric oxide and redox mechanisms in the immune response (2011, background): “tion, and the formation of new blood vessels [191, 234].”
- Efficient clearance of early apoptotic cells by human macrophages requires “M2c” polarization and MerTK induction (2012, background): “IL-10, TGF-b, and glucocorticoids are the factors currently classified as M2c stimuli (31).”
- IRF5 promotes inflammatory macrophage polarization and TH1-TH17 responses (2011, background): “, these cells are now referred to as M1 (classic) macrophages, which produce proinflammatory cytokines and mediate resistance to pathogens and contribute to tissue destruction, and M2 (alternative) macrophages, which produce anti-inflammatory cytokines and promote tissue repair and remodeling as wel”
- Characterization of phenotype markers and neuronotoxic potential of polarised primary microglia in vitro (2013, background): “Nomenclature of these phenotypes varies across the literature (Kreider et al., 2007; Martinez et al., 2008) but can be characterised into four main states, classically activated M1 with cytotoxic properties; M2a with an alternate activation and involved in repair and regeneration; M2b with an…”
- Exploring the full spectrum of macrophage activation (2008, background): “However, the M2 designation has rapidly expanded to include essentially all other types of macrophag”
- Targeting tumor-associated macrophages with anti-CSF-1R antibody reveals a strategy for cancer therapy. (2014, background): “This profile indicates an M2-like polarization of mac- rophages in the presence of CSF-1 (Geissmann et al., 2010; Martinez et al., 2008).”
- Macrophage plasticity, polarization, and function in health and disease (2018, background): “Pulmonarymacrophagesproduce a variety of factorswhich directly stimulate airway smooth muscle contractility and ECM degradation contributing to pathological airway remodeling (Murray et al., 2014; Wynn et al., 2013; Wynn & Ramalingam, 2012).”