TNF and increased intracellular iron alter macrophage polarization to a detrimental M1 phenotype in the injured spinal cord.

By A. Kroner, A. Greenhalgh, J. Zarruk, Rosmarini Passos dos Santos, M. Gaestel, S. David. Neuron, 2014

627 citations recorded by the source corpus.

Subfields: Immunology, Pathology and Forensic Medicine, Public Health, Environmental and Occupational Health

View Paper: https://www.semanticscholar.org/paper/c47cf9af6ef19232682050b9295e0ab86adabca7

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In Pathology and Forensic Medicine

Citations in the corpus

Microglia in the TBI Brain: The Good, The Bad, And The Dysregulated (2015, background): “Several soluble factors found in the lesion microenvironment, such as TNFα, IFNγ and lipocalin-2, can drive this M2 to M1 transition (Jang et al., 2013; Kroner et al., 2014).”
Inhibition of neuronal ferroptosis protects hemorrhagic brain. (2017, background): “Evidence indicates that iron and TNF-α can change the polarization of microglia (44), and that the”
The Reactive Oxygen Species in Macrophage Polarization: Reflecting Its Dual Role in Progression and Treatment of Human Diseases (2016, background): “Multiple signalling pathways and several cellular stimuli, such as cAMP [8], phospholipid [9], and irons [10], have been found involved in the functional polarization of macrophages.”
Spinal cord injury: molecular mechanisms and therapeutic interventions (2023, background): “In related studies on the mechanism of macrophage activation after SCI, an increase in intracellular iron and myelin debris could regulate the polarization of macrophages, promoting a harmful M1 phenotype.(92,93) The lipid catabolic pathway is another target for regulating the important functions of”
Revisiting the concept of CNS immune privilege (2015, background): “Do patients afflicted with MS and/or Alzheimer's disease exhibit specific changes in meningeal lymphatic vessels? If so, could these changes be indicative/predictive of disease? [93–97].”
Macrophage Polarization. (2017, background): “For example, TNF suppresses the ability of macrophages to contribute to healing damage in the spinal cord and is vital for the suppression of the normal homeostatic M2-like macrophages in adipose tissue (76, 77).”
Traumatic Spinal Cord Injury: An Overview of Pathophysiology, Models and Acute Injury Mechanisms (2019, background): “SCI studies have revealed that increased level of the proinflammatory cytokine, TNF-α, and intracellular accumulation of iron drives an M1-like proinflammatory phenotype in macrophages after injury (231).”
Alternatively activated microglia and macrophages in the central nervous system. (2015, background): “…Surface receptor Recognize the Fc portion of IgG (Fc gamma RIII) Yes Yes Yes Yes David and Kroner (2011), Hirai et al. (2013), Hu et al. (2012), Kroner et al. (2014) CD32 Surface receptor Recognize the Fc portion of IgG (Fc gamma RII) Yes Yes Yes Yes David and Kroner (2011), Hirai et al.…”
Spinal Cord Injury: Pathophysiology, Multimolecular Interactions, and Underlying Recovery Mechanisms (2020, background): “Post SCI the activation of B cells is suppressed, which leads to suppression of antibody production [131], but according to a study, the activity of B cells got influenced by the levels of injury, upper thoracic SCI retard antibody production however mid-thoracic injury produces no effect on antibod”
The Biology of Regeneration Failure and Success After Spinal Cord Injury. (2018, background): “(212) have presented a possible explanation as to how this M2 phenotype may be normally repressed.”