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Review
. 2010 May;30 Suppl 1(Suppl 1):S109-12.
doi: 10.1007/s10875-010-9404-7.

Immunoglobulin G: a potential treatment to attenuate neuroinflammation following spinal cord injury

Michael G Fehlings  1 , Dung H Nguyen
Affiliations
Review

Immunoglobulin G: a potential treatment to attenuate neuroinflammation following spinal cord injury

Michael G Fehlings et al. J Clin Immunol. 2010 May.

Abstract

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.

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Figures

Fig. 1
Fig. 1
Potential interactions of IgG with the neuroinflammatory response following SCI. Schematic diagram represents how the infiltration of microglia and leukocytes could exacerbate the initial damage. Microglia and leukocytes are recruited to the injury epicenter where they produce neurotoxic substances that cause neuronal and oligodendrocytic cell death in the secondary injury cascade. IgG has the potential to reduce the extent of secondary damage by interacting with microglia and leukocytes in the following mechanism: (1) inhibit microglia activation and reduce proinflammatory cytokine production, (2) inhibit leukocyte recruitment to the injury epicenter following SCI by acting on endothelial cells, and (3) inhibit leukocyte activation by upregulation of the inhibitory FcγIIB receptor. BBB blood-brain barrier, LIF leukemia inhibitory factor, ROS reactive oxygen species, NOS nitrous oxide synthase, MMPs matrix-metalloproteinases
See this image and copyright information in PMC

References

    1. Christopher and Dana Reeve Foundation. Paralysis facts and figures. http://www.christopherreeve.org/site/c.mtKZKgMWKwG/b.5184189/k.5587/Para.... Accessed Nov. 25, 2009.
    1. Baptise D, Fehlings M. Emerging drugs for spinal cord injury. Expert Opin Emerg Drugs. 2008;13(1):63–80. doi: 10.1517/14728214.13.1.63. - DOI - PubMed
    1. Tator C, Fehlings M. Review of the secondary injury theory of acute spinal cord trauma with emphasis on vascular mechanisms. J Neurosurg. 1991;75:15–26. doi: 10.3171/jns.1991.75.1.0015. - DOI - PubMed
    1. Profyris C, Cheema S, Zang D, Azari M, Boyle K, Petratos S. Degenerative and regenerative mechanisms governing spinal cord injury. Neurobiol Dis. 2004;15(3):415–36. doi: 10.1016/j.nbd.2003.11.015. - DOI - PubMed
    1. Donnelly DJ, Popovich PG. Inflammation and its role in neuroprotection, axonal regeneration and function recovery after spinal cord injury. Exp Neurol. 2008;209(2):378–88. doi: 10.1016/j.expneurol.2007.06.009. - DOI - PMC - PubMed

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