Introduction: Spinal cord injury (SCI) is caused by two related but mechanistically distinct events: the primary injury to the spinal cord is caused by a mechanic trauma; the secondary injury is a cascade of cellular and molecular events that exacerbates the initial damage.
Materials and methods: Neuroinflammation, an important event in the secondary injury cascade, is critical in the clearance of cellular debris after SCI. However, leukocytes and microglia, recruited to the injury site during neuroinflammation, can exacerbate the initial damage following SCI by secreting reactive oxygen species, matrix-metalloproteinase, and proinflammatory cytokines. Therefore, attenuating the activity of leukocytes and microglia is an attractive therapeutic strategy to reduce the neurological deficit associated with SCI.
Discussion: In this regard, immunoglobulin G (IgG) is a potential treatment candidate. IgG has been used clinically to treat autoimmune disease and has been demonstrated to attenuate the activities of leukocytes and microglia. In this review, we discuss the potential use of IgG for SCI based on the current understanding of the immune-modulating mechanism of IgG and the role of neuroinflammation in SCI.