The chemokine system in diverse forms of macrophage activation and polarization.

By A. Mantovani, A. Sica, S. Sozzani, P. Allavena, A. Vecchi, M. Locati. Trends in immunology, 2004

6,535 citations recorded by the source corpus.

Subfields: Immunology, Oncology

View Paper: https://www.semanticscholar.org/paper/fbf58da8ebd072bb1fcb43683a2bf6490fe79c31

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Immunology

1. A. Mantovani
2. A. Sica
3. S. Gordon
4. P. Allavena
5. F. Martínez
6. Subhra K. Biswas
7. Peter Libby
8. C. Garlanda

In Oncology

1. A. Mantovani
2. A. Sica
3. S. Gordon
4. F. Martínez
5. P. Allavena
6. Peter Libby
7. S. Badylak
8. C. Garlanda

Citations in the corpus

• From Monocytes to M1/M2 Macrophages: Phenotypical vs. Functional Differentiation (2014, background): “Moreover, M1 and M2 macrophages have distinct features in terms of chemokine production profiles (171), and iron and glucose metabolism (172, 173).”
• Mechanisms of foam cell formation in atherosclerosis (2017, background): “Typically, M2 macrophages secrete significant amounts of anti-inflammatory IL-10 and transforming growth factor (TGF)-β, contribute to wound healing, phagocytosis of apoptotic cells, tissue remodeling, angiogenesis, and carcinogenesis [25].”
• Role of tumor-associated macrophages in tumor progression and invasion (2006, background): “The capability to express distinct functional programs in response to different microenvironmental signals is a biological feature of macrophages, which is typically manifested in pathological conditions such as infections and cancer [10, 11].”
• A CREB-C/EBPβ cascade induces M2 macrophage-specific gene expression and promotes muscle injury repair (2009, background): “M2 macrophage polarization is induced by anti-inflammatory cytokines and growth factors, including IL-4, IL-10, and TGF- (3).”
• Tumor‐associated macrophages (TAM) as major players of the cancer‐related inflammation (2009, background): “, CCL17 and CCL22), which preferentially attract T cell subsets devoid of cytotoxic functions such as Treg and Th2 [23, 46].”
• Overview of General and Discriminating Markers of Differential Microglia Phenotypes (2020, background): “In such a comparison, the ratio IL-12high/IL- 10low could be a confirmation of M1 activation (Mantovani et al., 2004).”
• Pro-Resolving lipid mediators and Mechanisms in the resolution of acute inflammation (2014, background): “, 2001), resolvins (Rvs), and protectins (PDs) (Hong et al., 2003; Marcheselli et al., 2003; Serhan et al., 2000; Serhan et al., 2002).”
• Different tumor microenvironments contain functionally distinct subsets of macrophages derived from Ly6C(high) monocytes. (2010, background): “MHC II TAMs, possibly under the influence of hypoxia, had the highest gene expression of monocyte-recruiting chemokines, whereas chemokines that can recruit Th1, Th2, or natural killer cells, such as Cx3cl1, Ccl5, Cxcl9, Cxcl10, Cxcl11, Ccl17, and Ccl22 (41), were clearly upregulated in MHC II TAMs.”
• Phenotypic Switching of Adipose Tissue Macrophages With Obesity Is Generated by Spatiotemporal Differences in Macrophage Subtypes (2008, background): “One potential clue to understanding these diverse functions emerges from the evidence that macrophages can exist in different activation states with distinct properties (8).”
• IL-33 Amplifies the Polarization of Alternatively Activated Macrophages That Contribute to Airway Inflammation1 (2009, background): “Furthermore, a distinct chemokine profile, including CCL17 (TARC), CCL22 (MDC), and CCL24 (eotaxin-2), has been associated with AAM activation (5).”
• TNF and increased intracellular iron alter macrophage polarization to a detrimental M1 phenotype in the injured spinal cord. (2014, neutral): “…CCL2 59 M1 chemokine 0.03 (Mantovani et al., 2004) Csf2 GM-CSF 36 M1 inducer 0.004 (Martinez et al., 2006) Cxcl16 CXCL16 30 M1 chemokine* 0.0001 (Mantovani et al., 2004) Il15 IL-15 16 M1 cytokine* 0.01 (Martinez et al., 2006) Ccl19 CCL19 15 M1 chemokine* 0.04 (Mantovani et al., 2004) Il18 IL-18…”
• Macrophages in Tumor Microenvironments and the Progression of Tumors (2012, background): “Several studies reporting the use of “antimacrophage” approaches have primarily focused on counteracting monocyte chemokines and receptors as anticancer targets [10, 14, 36, 42].”
• Exosome-Based Cell-Cell Communication in the Tumor Microenvironment (2018, background): “…macrophages can be educated into Tumor-Associated Macrophages (TAMs) displaying M2 characteristics, promoting angiogenesis and releasing pro-tumorigenic growth factors, chemokines and cytokines (Mantovani et al., 2004; Rogers and Holen, 2011; Quatromoni and Eruslanov, 2012; Schiavoni et al., 2013).”
• Macrophage Polarization in Bacterial Infections (2008, background): “M2c, induced by IL-10 and glucocorticoid hormones (10).”