Repertoire of microglial and macrophage responses after spinal cord injury

By S. David, A. Kroner. Nature Reviews Neuroscience, 2011

1,359 citations recorded by the source corpus.

Subfields: Immunology, Neurology, Pathology and Forensic Medicine

View Paper: https://www.semanticscholar.org/paper/1883caa5135a9beaa0e9119879473f260bc4f9b9

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Citations in the corpus

Immune-responsive gene 1 protein links metabolism to immunity by catalyzing itaconic acid production (2013, background): “J Interferon Cytokine Res 29(1):55–67.”
The Biology of Regeneration Failure and Success After Spinal Cord Injury. (2018, background): “Further complicating this story is the innate heterogeneity of both normal microglia and macrophages as well as the heterogeneity of their responses to injury (82).”
Traumatic Spinal Cord Injury: An Overview of Pathophysiology, Models and Acute Injury Mechanisms (2019, background): “Inhibition of LAR and RPTPσ enhanced an anti-inflammatory environment after SCI by promoting the populations of pro-regenerative M2-like microglia/macrophages and regulatory T cells (241) that are known to promote repair process (224).”
Macrophage activation and its role in repair and pathology after spinal cord injury. (2015, background): “We now understand that SCI activates macrophages with different functional phenotypes (Kigerl et al., 2009; David and Kroner, 2011; Shechter and Schwartz, 2012; Ren and Young, 2013; Shin et al., 2013; Thawer et al., 2013).”
Neuroinflammation and M2 microglia: the good, the bad, and the inflamed (2014, background): “With spinal cord injury and traumatic brain injury, the domination of M1 microglia is mainly due to the high levels of proinflammatory cytokines present [60,68].”
Neuroinflammation: The Devil is in the Details (2016, positive): “Additionally, both brain and spinal cord injury involve an acute, beneficial initial inflammatory response (David and Kroner 2011; Woodcock and Morganti-Kossmann 2013) which becomes damaging should it persist too long.”
TNF and increased intracellular iron alter macrophage polarization to a detrimental M1 phenotype in the injured spinal cord. (2014, neutral): “…0.001 (David and Kroner, 2011; Martinez et al., 2006) Csf1 M-CSF 17 M2 inducer 0.003 (Martinez et al., 2006) Il13 IL13 4 M2a cytokine 0.03 (David and Kroner, 2011) Adipoq Adiponectin 40 M2 inducer 0.02 (Lovren et al., 2010) Ccl24 CCL24 8 M2 chemokine 0.04 (Mantovani et al., 2004) Il16…”
Alternatively activated microglia and macrophages in the central nervous system. (2015, background): “…David and Kroner (2011), Lee and Kim (2010), Mosser and Edwards (2008) CCL19 Chemokine Macrophage inflammatory protein-3-beta Yes Yes Yes Yes David and Kroner (2011), Gomez-Nicola et al. (2010) CCL20 Chemokine Macrophage inflammatory protein-3 alpha Yes Yes Yes Yes David and Kroner (2011),…”
Characterization of phenotype markers and neuronotoxic potential of polarised primary microglia in vitro (2013, background): “Decreased expression of the T-cell stimulating factor IL-12 has been considered a hallmark of an M2b phenotype (Mantovani et al., 2009, David and Kroner, 2011).”
Minocycline selectively inhibits M1 polarization of microglia (2013, background): “M2 microglia express different molecules, such as IL-4, arignase1, Ym1, CD206, and IL-10, and show neuroprotective effects.(8,9,11,12) It has recently been reported that M2 microglia markers are”
The biphasic function of microglia in ischemic stroke (2017, neutral): “Microglia polarization could either exacerbate damage or promote tissue repair, which is partially dependent on different pathophysiological conditions (David and Kroner, 2011; O’Neill and Hardie, 2013).”
Microglia in the TBI Brain: The Good, The Bad, And The Dysregulated (2015, background): “…functional role ofmicroglia in the injured brain and spinal cord has developed significantly in recent years, with strong support for dual beneficial and detrimental roles for microglia, resulting in tissue repair or neurodegeneration respectively (David and Kroner, 2011; Kumar and Loane, 2012).”