Spinal cord injury (SCI) causes long-lasting damage in the spinal cord that leads to paraparesis, paraplegia, quadriplegia and other lifetime disabilities. The emergence of antibody treatment has paved a new pathway for the management of SCI. In this current review, Professor Weijiang Zhao and Doctor Danyang Tang summarize the experimentally therapeutic application of antibodies in SCI.
Spinal cord injury (SCI) causes long-lasting damage in the spinal cord that leads to paraparesis, paraplegia, quadriplegia and other lifetime disabilities. The underlying mechanisms responsible for the failure of axonal regeneration after SCI remain only partially understood. Although a spectrum of medical treatments has been made available for this disease, the therapeutic effects remain disappointing. The emergence of antibody treatment has paved a new pathway for the management of SCI. In this current review, the authors summarize the application of antibodies in SCI in studies of myelin repair, neuroprotection, axon outgrowth, and anti-immune reaction.
For myelin repair, the therapeutic functions and underlying mechanisms for antibodies targeting inhibitory molecules such as Nogo-A, myelin-associated glycoprotein (MAG), Nogo-66 receptor (NgR), leucine rich repeat and Ig domain containing Nogo receptor interacting protein-1 (LINGO-1), Rho-associated protein kinase (Rock) pathway, repulsive guidance molecule (RGMa), as well as tenascin-R (Tn-R) are mainly reviewed. In addition, antibodies targeting glial scar formation-related molecules, including NG2 and transforming growth factor (TGF) are described. Antibodies against CD11d, tumor necrosis factor (TNF)-α, cytokine interleukin-6 (IL-6), nitric oxide (NO), integrin α4β1 and αDβ2, lysophosphatidic acid (LPA) and interleukin-4 (IL-4) are also reviewed as neuroprotective reagents. The authors also describe cell adhesion molecule L1 (L1CAM) antibody to promote neurite outgrowth. For anti-immune reaction treatment, the authors describe several antibodies that can inhibit the functions of either T cells or B cells during the progression of SCI. In the meantime, the combinatorial treatment of the antibody with other reagents or stem cell transplant, as well as antibodies against molecules contributing to SCI-related neuropathic pain is also reviewed.
Despite the significant limitations of antibody treatment, the authors are still confident about the future application of antibodies as a promising therapeutic means to counteract the damage caused by SCI.