Functional plasticity of macrophages: reversible adaptation to changing microenvironments
By R. Stout, J. Suttles. Journal of Leukocyte Biology, 2004
803 citations recorded by the source corpus.
Subfields: Immunology, Neurology
View Paper: https://www.semanticscholar.org/paper/0df836901fd8301e47af642ca9a4b55b31b6c329
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Citations in the corpus
- Microglia: active sensor and versatile effector cells in the normal and pathologic brain (2007, background): “In other words, distinct functional macrophage phenotypes may follow each other, as indicated by proof-of-principle experiments [ 33-36 ].”
- Kupffer Cells in the Liver (2013, positive): “Much of our understanding of macrophage plasticity comes from resident macrophages in adipose tissue and nontissue macrophages (16,132).”
- Macrophages Sequentially Change Their Functional Phenotype in Response to Changes in Microenvironmental Influences1 (2005, background): “Thus the age-related inflammatory deficiencies of macrophages may be responsive at least transiently to cytokine therapy (21).”
- Macrophages and Tissue Injury: Agents of Defense or Destruction? (2011, background): “This illustrates the plasticity of macrophages and their ability to modulate their responses as a consequence of a changing microenvironment (5, 8, 10).”
- Oxidative metabolism and PGC-1beta attenuate macrophage-mediated inflammation. (2006, background): “For example, the Th1-type cytokine, IFNγ, primes macrophages to increase production of proinflammatory cytokines, reactive oxygen species and nitric oxide for safe clearance of intracellular pathogens (Gordon, 2003;Stout and Suttles, 2004).”
- Obesity induces a phenotypic switch in adipose tissue macrophage polarization. (2007, background): “normal and inflamed tissues (33), we hypothesized that ATMs are differentially activated depending on the degree of adiposity and, further, that in addition to quantitative differences, qualitative differences exist between ATMs in lean and obese animals.”
- AMP-activated protein kinase promotes macrophage polarization to an anti-inflammatory functional phenotype (2008, neutral): “Indeed, the array of possible functional outcomes of macrophage activation is quite broad (32), and we and others have demonstrated that macrophages can rapidly change their functional profile, both in vitro and in vivo, in response to changes in the microenvironment (39–41).”
- Protective and pathogenic functions of macrophage subsets (2011, background): “Indeed, numerous studies have documented flexibility in their programming, with macrophages switching from one functional phenotype to another in response to the variable microenvironmental signals of the local milie”
- Macrophage-mediated inflammation in metabolic disease (2011, background): “Although segregating macrophages into these two states is experimentally very useful, it also has its limitations, as macrophage phenotypes in vivo exhibit plasticity across the entire spectrum of activation states that are encompassed by the M1 and M2 nomenclatur”
- Biomaterial based modulation of macrophage polarization: A review and suggested design principles (2015, background): “This is emphasized by the contrasting gene expression during early and late stages of the FBR [24], as well as their ability to adapt functionality in response to the temporal presentation of stimuli [25].”
- Macrophage Polarization in Bacterial Infections (2008, background): “Consequently, macrophages display progressive functional changes resulting from changes in the microenvironment (12).”
- Identification of two distinct macrophage subsets with divergent effects causing either neurotoxicity or regeneration in the injured mouse spinal cord (2009, background): “, 2007), and recent data suggest that a fully differentiated macrophage subpopulation can reversibly change its phenotype and function in response to signals in the microenvironment (Stout and Suttles, 2004; Mosser and Edwards, 2008).”