Macrophage plasticity and interaction with lymphocyte subsets: cancer as a paradigm
By Subhra K. Biswas, A. Mantovani. Nature Immunology, 2010
3,752 citations recorded by the source corpus.
Subfields: Immunology
View Paper: https://www.semanticscholar.org/paper/2242ea323b9acd7babc4545a81cf7c978797d374
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Citations in the corpus
- Vascular normalizing doses of antiangiogenic treatment reprogram the immunosuppressive tumor microenvironment and enhance immunotherapy (2012, background): “Within breast cancer lesions, TAMs represent the dominant myeloid cell population and usually have an immunosuppressiveM2-like phenotype associated with the hypoxic tumor microenvironment (14, 17, 18).”
- Tumor associated macrophages and neutrophils in cancer. (2013, background): “Moreover, they suppress Th1 adaptive immunity, participate in the resolution of inflammation, in the protection against parasites, promote wound healing, angiogenesis and tissue remodeling (Biswas and Mantovani 2010).”
- Targeting tumor-associated macrophages with anti-CSF-1R antibody reveals a strategy for cancer therapy. (2014, background): “The tumor-promoting function of TAMs is based on their capacity to secrete proangiogenic and growth factors, as well as to potently suppress T cell effector function by releasing immunosuppressive cytokines and affecting their metabolism (Wynn et al., 2013; Biswas and Mantovani 2010; Gordon and Mart”
- Prognostic Significance of Tumor-Associated Macrophages in Solid Tumor: A Meta-Analysis of the Literature (2012, background): “Differentiation of the M2 macrophages is induced by IL-4 or IL-13 and associated with parasite clearance, wound healing and dampen immune responses [5].”
- Pathophysiology of Myocardial Infarction (2015, neutral): “Traditionally, two major macrophage subsets are recognized (243): the classically activated M1 macrophages that predominantly secrete proinflammatory mediators, and the alternatively activated M2 macrophages that secrete anti-inflammatory cytokines (such as IL-10) and express mediators that terminat”
- The tumor microenvironment underlies acquired resistance to CSF1R inhibition in gliomas (2016, methodology): “Given the similarities in alternative activation between Veh and Reb TAMs according to the M1/M2-like paradigm (26), yet clear differences in drug response between treatment-naïve and rebound tumors, we next used a more fine-tuned approach to defining macrophage phenotype.”
- Neuroinflammation and M2 microglia: the good, the bad, and the inflamed (2014, background): “Although tumor-associated macrophages are an area of intense research [53], they are beyond the scope of this review.”
- Transcriptome-Based Network Analysis Reveals a Spectrum Model of Human Macrophage Activation (2014, background): “…Trupti D. Gohel,1 Martina Emde,1 Lisa Schmidleithner,1 Hariharasudan Ganesan,1 Andrea Nino-Castro,1 Michael R. Mallmann,1 Larisa Labzin,2 Heidi Theis,1 Michael Kraut,1 Marc Beyer,1 Eicke Latz,2,3,4 Tom C. Freeman,5 Thomas Ulas,1 and Joachim L. Schultze1,* 1Genomics and Immunoregulation,…”