Quantitative analysis of cellular inflammation after traumatic spinal cord injury: evidence for a multiphasic inflammatory response in the acute to chronic environment.

By K. Beck, Hal X. Nguyen, M. Galvan, Desiree Salazar, T. Woodruff, A. Anderson. Brain : a journal of neurology, 2010

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The Biology of Regeneration Failure and Success After Spinal Cord Injury. (2018, background): “Persistent permeability of the BSCB allows for the chronic infiltration of monocytes into the cord (30, 202), which further potentiates the inhibitory effects of the lesion (49).”
Traumatic Spinal Cord Injury: An Overview of Pathophysiology, Models and Acute Injury Mechanisms (2019, background): “Of note, antibody mediated injury is regulated through complement activation as well as macrophages/microglia that express immunoglobulin receptors (193, 255).”
Macrophage activation and its role in repair and pathology after spinal cord injury. (2015, background): “In addition, neutrophil accumulation begins within hours of SCI and, regardless of species, peaks within the normal timeframe of the inflammatory phase (1–3 days post-injury) (Kigerl et al., 2006; Beck et al., 2010; Prüss et al., 2011).”
Spinal Cord Injury: Pathophysiology, Multimolecular Interactions, and Underlying Recovery Mechanisms (2020, background): “The scar size is controlled by the interaction of Signal transducer and activator of transcription 3 (STAT3), Suppressors of Cytokine Signaling-3 (SOCS3), or Nuclear factor-kappa B (NF-kB), and the organisation of the astrocyte scar is accomplished by the IL-6 receptor-STAT3 signalling system [57,58”