![]() Our findings support the consensus that future neuroprotective immunotherapies should aim to selectively neutralize detrimental immune signaling while sustaining pro-regenerative processes. Findings were verified in postmortem tissue from individuals with SCI. By 21 and 28 days after SCI, the lesion core was populated by galectin-3 +, CD68 +, and CD11b + microglia/macrophages, surrounded by a glial scar consisting of GFAP + astrocytes. Microglial/macrophage expression of Arg1 increased from 1–7 days after SCI, followed by an increase in Itgam, Cx3cr1, and P2ry12, which remained elevated throughout the study. The acute phase was dominated by the infiltration of granulocytes and macrophages. TNFR1 and TNFR2 levels increased in the delayed phase and were found preferentially on neurons and glial cells, respectively. In the acute phase, TNF expression increased in glial cells and neuron-like cells, followed by infiltrating immune cells. ![]() We examined activation, recruitment, and polarization of microglia and infiltrating immune cells, focusing specifically on tumor necrosis factor (TNF) and its receptors TNFR1 and TNFR2. We subjected C57BL/6J mice to SCI and investigated inflammatory reactions. Understanding the role of the inflammatory response in SCI requires insight into the temporal and cellular synthesis of inflammatory mediators. Spinal cord injury (SCI) initiates detrimental cellular and molecular events that lead to acute and delayed neuroinflammation.
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