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Microglial and macrophage polarization—new prospects for brain repair
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“These cells are inherently heterogeneous and display remarkable functional plasticity, categorizing into two major phenotypes: M1 and M2 [3, 4].”
From miR-223 accelerates lipid droplets clearance in microglia following spinal cord injury by upregulating ABCA1 (2024) · cites this paper as [4]
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Exploring the full spectrum of macrophage activation
Mosser, D. M., & Edwards, J. P. (2008) · Nature Reviews Immunology · doi:10.1038/nri2448 · Cited by 9,144
Resting microglial cells are highly dynamic surveillants of brain parenchyma in vivo
Nimmerjahn, A., Kirchhoff, F., & Helmchen, F. (2005) · Science · doi:10.1126/science.1110647 · Cited by 5,827
Synaptic Pruning by Microglia Is Necessary for Normal Brain Development
Paolicelli, R. C., Bolasco, G., Pagani, F., Maggi, L., Scianni, M., Panzanelli, P., Giustetto, M., Ferreira, T. A., Guiducci, E., Dumas, L., et al. (2011) · Science · doi:10.1126/science.1202529 · Cited by 4,244
Microglia Sculpt Postnatal Neural Circuits in an Activity and Complement-Dependent Manner
Schafer, D. P., Lehrman, E. K., Kautzman, A. G., Koyama, R., Mardinly, A. R., Yamasaki, R., Ransohoff, R. M., Greenberg, M. E., Barres, B. A., & Stevens, B. (2012) · Neuron · doi:10.1016/j.neuron.2012.03.026 · Cited by 4,089
ATP mediates rapid microglial response to local brain injury in vivo
Davalos, D., Grutzendler, J., Yang, G., Kim, J. V., Zuo, Y., Jung, S., Littman, D. R., Dustin, M. L., & Gan, W.-B. (2005) · Nature Neuroscience · doi:10.1038/nn1472 · Cited by 3,913
M2 microglia and macrophages drive oligodendrocyte differentiation during CNS remyelination
Miron, V. E., Boyd, A., Zhao, J.-W., Yuen, T. J., Ruckh, J. M., Shadrach, J. L., van Wijngaarden, P., Wagers, A. J., Williams, A., Franklin, R. J. M., et al. (2013) · Nature Neuroscience · doi:10.1038/nn.3469 · Cited by 1,777
Synaptic scaling mediated by glial TNF-α
Stellwagen, D., & Malenka, R. C. (2006) · Nature · doi:10.1038/nature04671 · Cited by 1,715
Inflammation and wound healing: the role of the macrophage
Koh, T. J., & DiPietro, L. A. (2011) · Expert Reviews in Molecular Medicine · doi:10.1017/s1462399411001943 · Cited by 1,667
Inflammation is detrimental for neurogenesis in adult brain
Ekdahl, C. T., Claasen, J.-H., Bonde, S., Kokaia, Z., & Lindvall, O. (2003) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.2234031100 · Cited by 1,559
Ponomarev, E. D., Veremeyko, T., Barteneva, N., Krichevsky, A. M., & Weiner, H. L. (2011) · Nature Medicine · doi:10.1038/nm.2266 · Cited by 787
Research works printed but not linked: 95
- Lo, E. H. Degeneration and repair in central nervous system disease. Nat. Med. 16, 1205–1209 (2010). · DOI
- Chu, M. et al. Focal cerebral ischemia activates neurovascular restorative dynamics in mouse brain. Front. Biosci. (Elite Ed.) 4, 1926–1936 (2012). · DOI
- Gutiérrez-Fernández, M. et al. Trophic factors and cell therapy to stimulate brain repair after ischaemic stroke. J. Cell. Mol. Med. 16, 2280–2290 (2012). · DOI
- Zhang, J. H. et al. The vascular neural network—a new paradigm in stroke pathophysiology. Nat. Rev. Neurol. 8, 711–716 (2012). · DOI
- Hanisch, U. K. & Kettenmann, H. Microglia: active sensor and versatile effector cells in the normal and pathologic brain. Nat. Neurosci. 10, 1387–1394 (2007). · DOI · Paper page
- Kwon, M. J. et al. Contribution of macrophages to enhanced regenerative capacity of dorsal root ganglia sensory neurons by conditioning injury. J. Neurosci. 33, 15095–15108 (2013). · DOI
- Liu, Z. et al. Chronic treatment with minocycline preserves adult new neurons and reduces functional impairment after focal cerebral ischemia. Stroke 38, 146–152 (2007). · DOI
- David, S. & Kroner, A. Repertoire of microglial and macrophage responses after spinal cord injury. Nat. Rev. Neurosci. 12, 388–399 (2011). · DOI · Paper page
- Moore, K. J., Sheedy, F. J. & Fisher, E. A. Macrophages in atherosclerosis: a dynamic balance. Nat. Rev. Immunol. 13, 709–721 (2013). · DOI · Paper page
- Boche, D., Perry, V. H. & Nicoll, J. A. Review: activation patterns of microglia and their identification in the human brain. Neuropathol. Appl. Neurobiol. 39, 3–18 (2013). · DOI
- Hu, X. et al. Microglia/macrophage polarization dynamics reveal novel mechanism of injury expansion after focal cerebral ischemia. Stroke 43, 3063–3070 (2012). · DOI
- Wang, G. et al. Microglia/macrophage polarization dynamics in white matter after traumatic brain injury. J. Cereb. Blood Flow Metab. 33, 1864–1874 (2013). · DOI · Paper page
- Kigerl, K. A. et al. Identification of two distinct macrophage subsets with divergent effects causing either neurotoxicity or regeneration in the injured mouse spinal cord. J. Neurosci. 29, 13435–13444 (2009). · DOI · Paper page
- Thiel, A. & Heiss, W. D. Imaging of microglia activation in stroke. Stroke 42, 507–512 (2011). · DOI
- Perego, C., Fumagalli, S. & De Simoni, M. G. Temporal pattern of expression and colocalization of microglia/macrophage phenotype markers following brain ischemic injury in mice. J. Neuroinflammation 8, 174 (2011). · DOI
- Girard, S. et al. Microglia and macrophages differentially modulate cell death after brain injury caused by oxygen-glucose deprivation in organotypic brain slices. Glia 61, 813–824 (2013). · DOI
- Durafourt, B. A. et al. Comparison of polarization properties of human adult microglia and blood-derived macrophages. Glia 60, 717–727 (2012). · DOI
- Nakayama, D. et al. Injury-induced neural stem/progenitor cells in post-stroke human cerebral cortex. Eur. J. Neurosci. 31, 90–98 (2010). · DOI
- Lu, K. T. et al. Hippocampal neurogenesis after traumatic brain injury is mediated by vascular endothelial growth factor receptor-2 and the Raf/MEK/ERK cascade. J. Neurotrauma 28, 441–450 (2011). · DOI
- Hart, A. D., Wyttenbach, A., Perry, V. H. & Teeling, J. L. Age related changes in microglial phenotype vary between CNS regions: grey versus white matter differences. Brain Behav. Immun. 26, 754–765 (2012). · DOI · Paper page
- Norden, D. M. & Godbout, J. P. Review: microglia of the aged brain: primed to be activated and resistant to regulation. Neuropathol. Appl. Neurobiol. 39, 19–34 (2013). · DOI · Paper page
- Hickman, S. E. et al. The microglial sensome revealed by direct RNA sequencing. Nat. Neurosci. 16, 1896–1905 (2013). · DOI · Paper page
- Jung, S. & Schwartz, M. Non-identical twins—microglia and monocyte-derived macrophages in acute injury and autoimmune inflammation. Front. Immunol. 3, 89 (2012). · DOI
- Butovsky, O. et al. Microglia activated by IL-4 or IFN-γ differentially induce neurogenesis and oligodendrogenesis from adult stem/progenitor cells. Mol. Cell Neurosci. 31, 149–160 (2006). · DOI · Paper page
- Roughton, K., Andreasson, U., Blomgren, K. & Kalm, M. Lipopolysaccharide-induced inflammation aggravates irradiation-induced injury to the young mouse brain. Dev. Neurosci. 35, 406–415 (2013). · DOI
- Nikolakopoulou, A. M., Dutta, R., Chen, Z., Miller, R. H. & Trapp, B. D. Activated microglia enhance neurogenesis via trypsinogen secretion. Proc. Natl Acad. Sci. USA 110, 8714–8719 (2013). · DOI
- Yan, Y. P., Lang, B. T., Vemuganti, R. & Dempsey, R. J. Galectin-3 mediates post-ischemic tissue remodeling. Brain Res. 1288, 116–124 (2009). · DOI
- Choi, Y. S., Cho, H. Y., Hoyt, K. R., Naegele, J. R. & Obrietan, K. IGF-1 receptor-mediated ERK/MAPK signaling couples status epilepticus to progenitor cell proliferation in the subgranular layer of the dentate gyrus. Glia 56, 791–800 (2008). · DOI
- Kim, B. J. et al. Reduced neurogenesis after suppressed inflammation by minocycline in transient cerebral ischemia in rat. J. Neurol. Sci. 279, 70–75 (2009). · DOI
- Cafferty, W. B., McGee, A. W. & Strittmatter, S. M. Axonal growth therapeutics: regeneration or sprouting or plasticity? Trends Neurosci. 31, 215–220 (2008). · DOI
- Horn, K. P., Busch, S. A., Hawthorne, A. L., van Rooijen, N. & Silver, J. Another barrier to regeneration in the CNS: activated macrophages induce extensive retraction of dystrophic axons through direct physical interactions. J. Neurosci. 28, 9330–9341 (2008). · DOI
- Kitayama, M., Ueno, M., Itakura, T. & Yamashita, T. Activated microglia inhibit axonal growth through RGMa. PLoS ONE 6, e25234 (2011). · DOI
- Yin, Y. et al. Oncomodulin is a macrophage-derived signal for axon regeneration in retinal ganglion cells. Nat. Neurosci. 9, 843–852 (2006). · DOI
- Yin, Y. et al. Oncomodulin links inflammation to optic nerve regeneration. Proc. Natl Acad. Sci. USA 106, 19587–19592 (2009). · DOI
- Wake, H., Moorhouse, A. J., Jinno, S., Kohsaka, S. & Nabekura, J. Resting microglia directly monitor the functional state of synapses in vivo and determine the fate of ischemic terminals. J. Neurosci. 29, 3974–3980 (2009). · DOI · Paper page
- Zhan, Y. et al. Deficient neuron–microglia signaling results in impaired functional brain connectivity and social behavior. Nat. Neurosci. 17, 400–406 (2014). · DOI · Paper page
- Stevens, B. et al. The classical complement cascade mediates CNS synapse elimination. Cell 131, 1164–1178 (2007). · DOI · Paper page
- Medina, R. J. et al. Myeloid angiogenic cells act as alternative M2 macrophages and modulate angiogenesis through interleukin-8. Mol. Med. 17, 1045–1055 (2011). · DOI
- Zajac, E. et al. Angiogenic capacity of M1- and M2-polarized macrophages is determined by the levels of TIMP-1 complexed with their secreted proMMP-9. Blood 122, 4054–4067 (2013). · DOI
- Welser, J. V., Li, L. & Milner, R. Microglial activation state exerts a biphasic influence on brain endothelial cell proliferation by regulating the balance of TNF and TGF-β1. J. Neuroinflammation 7, 89 (2010). · DOI
- Flögel, U. et al. In vivo monitoring of inflammation after cardiac and cerebral ischemia by fluorine magnetic resonance imaging. Circulation 118, 140–148 (2008). · DOI
- Venneti, S., Lopresti, B. J. & Wiley, C. A. Molecular imaging of microglia/macrophages in the brain. Glia 61, 10–23 (2013). · DOI
- Chhor, V. et al. Characterization of phenotype markers and neuronotoxic potential of polarised primary microglia in vitro. Brain Behav. Immun. 32, 70–85 (2013). · DOI
- Rolls, A. et al. Two faces of chondroitin sulfate proteoglycan in spinal cord repair: a role in microglia/macrophage activation. PLoS Med. 5, e171 (2008). · DOI
- Verma, S., Nakaoke, R., Dohgu, S. & Banks, W. A. Release of cytokines by brain endothelial cells: a polarized response to lipopolysaccharide. Brain Behav. Immun. 20, 449–455 (2006). · DOI
- Biswas, S. K. & Mantovani, A. Macrophage plasticity and interaction with lymphocyte subsets: cancer as a paradigm. Nat. Immunol. 11, 889–896 (2010). · DOI · Paper page
- Beers, D. R. et al. Endogenous regulatory T lymphocytes ameliorate amyotrophic lateral sclerosis in mice and correlate with disease progression in patients with amyotrophic lateral sclerosis. Brain 134, 1293–1314 (2011). · DOI
- Starossom, S. C. et al. Galectin-1 deactivates classically activated microglia and protects from inflammation-induced neurodegeneration. Immunity 37, 249–263 (2012). · DOI
- Jiang, M. H. et al. Substance P induces M2-type macrophages after spinal cord injury. Neuroreport 23, 786–792 (2012). · DOI
- Rocher, C. & Singla, D. K. SMAD–PI3K–Akt–mTOR pathway mediates BMP-7 polarization of monocytes into M2 macrophages. PLoS ONE 8, e84009 (2013). · DOI
- Gong, D. et al. TGFβ signaling plays a critical role in promoting alternative macrophage activation. BMC Immunol. 13, 31 (2012). · DOI
- Maiorino, C. et al. Lentiviral-mediated administration of IL-25 in the CNS induces alternative activation of microglia. Gene Ther. 20, 487–96 (2013). · DOI
- Sica, A. & Bronte, V. Altered macrophage differentiation and immune dysfunction in tumor development. J. Clin. Invest. 117, 1155–1166 (2007). · DOI
- Qin, H. et al. SOCS3 deficiency promotes M1 macrophage polarization and inflammation. J. Immunol. 189, 3439–3448 (2012). · DOI
- Martinez-Nunez, R. T., Louafi, F. & Sanchez-Elsner, T. The interleukin 13 (IL-13) pathway in human macrophages is modulated by microRNA-155 via direct targeting of interleukin 13 receptor α1 (IL13Rα1). J. Biol. Chem. 286, 1786–1794 (2011). · DOI
- Sheldon, K. E. et al. Shaping the murine macrophage phenotype: IL-4 and cyclic AMP synergistically activate the arginase I promoter. J. Immunol. 191, 2290–2298 (2013). · DOI
- Koscsó, B. et al. Adenosine augments IL-10-induced STAT3 signaling in M2c macrophages. J. Leukoc. Biol. 94, 1309–1315 (2013). · DOI
- Qin, H. et al. Signal transducer and activator of transcription-3/suppressor of cytokine signaling-3 (STAT3/SOCS3) axis in myeloid cells regulates neuroinflammation. Proc. Natl Acad. Sci. USA 109, 5004–5009 (2012). · DOI
- Weis, N., Weigert, A., von Knethen, A. & Brüne, B. Heme oxygenase-1 contributes to an alternative macrophage activation profile induced by apoptotic cell supernatants. Mol. Biol. Cell 20, 1280–1288 (2009). · DOI
- Sanson, M., Distel, E. & Fisher, E. A. HDL induces the expression of the M2 macrophage markers arginase 1 and Fizz-1 in a STAT6-dependent process. PLoS ONE 8, e74676 (2013). · DOI
- Bouhlel, M. A. et al. PPARγ activation primes human monocytes into alternative M2 macrophages with anti-inflammatory properties. Cell Metab. 6, 137–143 (2007). · DOI · Paper page
- Hasegawa-Moriyama, M. et al. Peroxisome proliferator-activated receptor-γ agonist rosiglitazone attenuates inflammatory pain through the induction of heme oxygenase-1 in macrophages. Pain 154, 1402–1412 (2013). · DOI
- Zhao, X. et al. Hematoma resolution as a target for intracerebral hemorrhage treatment: role for peroxisome proliferator-activated receptor γ in microglia/macrophages. Ann. Neurol. 61, 352–362 (2007). · DOI
- Satoh, T. et al. The Jmjd3–Irf4 axis regulates M2 macrophage polarization and host responses against helminth infection. Nat. Immunol. 11, 936–944 (2010). · DOI · Paper page
- Krausgruber, T. et al. IRF5 promotes inflammatory macrophage polarization and TH1–TH17 responses. Nat. Immunol. 12, 231–238 (2011). · DOI
- Xu, H. et al. Notch–RBP-J signaling regulates the transcription factor IRF8 to promote inflammatory macrophage polarization. Nat. Immunol. 13, 642–650 (2012). · DOI
- Ruffell, D. et al. A CREB-C/EBPβ cascade induces M2 macrophage-specific gene expression and promotes muscle injury repair. Proc. Natl Acad. Sci. USA 106, 17475–17480 (2009). · DOI · Paper page
- Ponomarev, E. D., Veremeyko, T. & Weiner, H. L. MicroRNAs are universal regulators of differentiation, activation, and polarization of microglia and macrophages in normal and diseased CNS. Glia 61, 91–103 (2013). · DOI · Paper page
- Cai, X. et al. Re-polarization of tumor-associated macrophages to pro-inflammatory M1 macrophages by microRNA-155. J. Mol. Cell Biol. 4, 341–343 (2012). · DOI
- Schulte, L. N., Westermann, A. J. & Vogel, J. Differential activation and functional specialization of miR-146 and miR-155 in innate immune sensing. Nucleic Acids Res. 41, 542–553 (2013). · DOI
- Guo, S. et al. IRF4 is a novel mediator for neuronal survival in ischaemic stroke. Cell Death Differ. 21, 888–903 (2014). · DOI
- Xiang, M. et al. Interferon regulatory factor 8 protects against cerebral ischaemic-reperfusion injury. J. Neurochem. 129, 988–1001 (2014). · DOI
- Hou, Y. C. et al. Preventive effect of silymarin in cerebral ischemia-reperfusion-induced brain injury in rats possibly through impairing NF-κB and STAT-1 activation. Phytomedicine 17, 963–973 (2010). · DOI
- Willemen, H. L. et al. MicroRNA-124 as a novel treatment for persistent hyperalgesia. J. Neuroinflammation 9, 143 (2012). · DOI · Paper page
- Desestret, V. et al. In vitro and in vivo models of cerebral ischemia show discrepancy in therapeutic effects of M2 macrophages. PLoS ONE 8, e67063 (2013). · DOI
- Mikita, J. et al. Altered M1/M2 activation patterns of monocytes in severe relapsing experimental rat model of multiple sclerosis. Amelioration of clinical status by M2 activated monocyte administration. Mult. Scler. 17, 2–15 (2011). · DOI · Paper page
- Zhu, W. et al. Insulin growth factor-1 gene transfer enhances neurovascular remodeling and improves long-term stroke outcome in mice. Stroke 39, 1254–1261 (2008). · DOI
- Courties, G. et al. In vivo silencing of the transcription factor IRF5 reprograms the macrophage phenotype and improves infarct healing. J. Am. Coll. Cardiol. 63, 1556–1566 (2014). · DOI
- Hall, J. L. & Wei, L. N. Could silencing IRF5 improve healing of a myocardial infarct through the reprogramming of the macrophage population? J. Am. Coll. Cardiol 63, 1567–1568 (2014). · DOI
- Eames, H. L. et al. KAP1/TRIM28: an inhibitor of IRF5 function in inflammatory macrophages. Immunobiology 217, 1315–1324 (2012). · DOI
- Xiong, X. et al. Increased brain injury and worsened neurological outcome in interleukin-4 knockout mice after transient focal cerebral ischemia. Stroke 42, 2026–2032 (2011). · DOI
- Boehler, R. et al. Lentivirus delivery of IL-10 to promote and sustain macrophage polarization towards an anti-inflammatory phenotype. Biotechnol. Bioeng. 111, 1210–1221 (2014). · DOI
- Zhao, B. Q. et al. Role of matrix metalloproteinases in delayed cortical responses after stroke. Nat. Med. 12, 441–445 (2006). · DOI
- Hanania, R. et al. Classically activated macrophages use stable microtubules for matrix metalloproteinase-9 (MMP-9) secretion. J. Biol. Chem. 287, 8468–8483 (2012). · DOI
- Komohara, Y., Ohnishi, K., Kuratsu, J. & Takeya, M. Possible involvement of the M2 anti-inflammatory macrophage phenotype in growth of human gliomas. J. Pathol. 216, 15–24 (2008). · DOI · Paper page
- Planas, A. M., Justicia, C. & Ferrer, I. Stat1 in developing and adult rat brain. Induction after transient focal ischemia. Neuroreport 8, 1359–1362 (1997). · DOI
- Wu, Y., Yang, L., Mei, X. & Yu, Y. Selective inhibition of STAT1 reduces spinal cord injury in mice. Neurosci. Lett. 580, 7–11 (2013). · DOI
- Liu, D. Z. et al. Brain and blood microRNA expression profiling of ischemic stroke, intracerebral hemorrhage, and kainate seizures. J. Cereb. Blood Flow Metab. 30, 92–101 (2010). · DOI
- Luo, Y. et al. Neuroprotection against focal ischemic brain injury by the peroxisome proliferator-activated receptor-γ agonist rosiglitazone. J. Neurochem. 97, 435–448 (2006). · DOI
- Erdö, F., Trapp, T., Mies, G. & Hossmann, K. A. Immunohistochemical analysis of protein expression after middle cerebral artery occlusion in mice. Acta Neuropathol. 107, 127–136 (2004). · DOI
- Shrivastava, K. et al. Temporal expression of cytokines and signal transducer and activator of transcription factor 3 activation after neonatal hypoxia/ischemia in mice. Dev. Neurosci. 35, 212–225 (2013). · DOI
- Bouhy, D. et al. Delayed GM-CSF treatment stimulates axonal regeneration and functional recovery in paraplegic rats via an increased BDNF expression by endogenous macrophages. FASEB J. 20, 1239–1241 (2006). · DOI
- Batchelor, P. E. et al. Macrophages and microglia produce local trophic gradients that stimulate axonal sprouting toward but not beyond the wound edge. Mol. Cell. Neurosci. 21, 436–453 (2002). · DOI
- Ardelt, A. A., Bhattacharyya, B. J., Belmadani, A., Ren, D. & Miller, R. J. Stromal derived growth factor-1 (CXCL12) modulates synaptic transmission to immature neurons during post-ischemic cerebral repair. Exp. Neurol. 248, 246–253 (2013). · DOI
- Yan, Y. P., Lang, B. T., Vemuganti, R. & Dempsey, R. J. Osteopontin is a mediator of the lateral migration of neuroblasts from the subventricular zone after focal cerebral ischemia. Neurochem. Int. 55, 826–832 (2009). · DOI
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Zhao, Y., Mu, H., Huang, Y., Li, S., Wang, Y., Stetler, R. A., Bennett, M. V. L., Dixon, C. E., Chen, J., & Shi, Y. (2022) · Journal of Neuroinflammation · doi:10.1186/s12974-022-02563-2 · Cited by 47
Self-citationOu, Z., Cheng, Y., Ma, H., Chen, K., Lin, Q., Chen, J., Guo, R., Huang, Z., Cheng, Q., Alaeiilkhchi, N., et al. (2024) · Journal of Translational Medicine · doi:10.1186/s12967-024-05480-5 · Cited by 23
Self-citationXie, M., Wang, T., Feng, J., Ma, D., Feng, L., & Hao, Y. (2025) · Current Neuropharmacology · doi:10.2174/1570159x23666250225091729 · Cited by 7
Metadata
- Authors
- Hu, X., Leak, R. K., Shi, Y., Suenaga, J., Gao, Y., Zheng, P., & Chen, J.
- Venue
- Nature Reviews Neurology
- Published
- 2014-11-11
- Volume
- 11
- Issue
- 1
- Pages
- 56-64
- ISSN
- 1759-4758
- 1759-4766
- PMC
- PMC4395497
- Cited by
- 1,366
- References
- 20
- Language
- en
- Licence
- www.springer.com/tdm (tdm)
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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