Immunomodulation as a neuroprotective strategy after spinal cord injury

• Published in: Neural regeneration research Vol. 13; no. 3; pp. 423 - 424
• Main Authors: Monteiro, Susana, Salgado, António, Silva, Nuno
• Format: Journal Article
• Language: English
• Published: India Wolters Kluwer India Pvt. Ltd 01.03.2018; Medknow Publications and Media Pvt. Ltd; Medknow Publications & Media Pvt. Ltd; Life and Health Sciences Research Institute (ICVS), School of Medicine, University of Minho, Campus de Gualtar, Braga, Portugal; ICVS/3B's – PT Government Associate Laboratory, Braga/Guimar?es, Portugal; Medknow Publications & Media Pvt Ltd
• Subjects: Analysis; Anti-inflammatory agents; Biomedical materials; Care and treatment; Chemokines; Complications and side effects; Cytokines; Dosage and administration; Genotype & phenotype; Immune response; Inflammation; Nervous system; Spinal cord injuries; Stem cells
• ISSN: 1673-5374; 1876-7958
• DOI: 10.4103/1673-5374.228722

The infiltration of immune cells within the nervous system parenchyma held a long-lasting bad reputation based on other neurological diseases whose etiology is characterized by an abnormal immune infiltration into the central nervous system (CNS) parenchyma. [...]particular anatomical features of the CNS that reduce neuroimmune interactions, such as the presence of barriers (blood-brain barrier, blood-spinal cord barrier and the choroid plexus-barrier) sustain the notion that CNS tissue should be protected from immune cells to maintain its homeostasis and integrity. [...]the only approved therapy for treating spinal cord injury is methylprednisolone, a potent anti-inflammatory drug. The local administration of TLR2 agonist boosts macrophage reaction while protecting the tissue after SCI (Gensel et al., 2015) demonstrating the importance of local molecular signals for macrophages engaging activation phenotypes associated with tissue repair. Another demonstration on the importance of the molecular environment for the type of immune response to SCI is the study by Kwon et al. showing that the presence of the chemokine, chemokine (C-C motif) ligand 2 (CCL2), at the injury drives a proregenerative activation phenotype by macrophages (Kwon et al., 2015).