Spinal cord injury (SCI) has a significant impact on the quality and expectancy of life. It also carries a heavy economic burden, with considerable costs associated with primary care and loss of income. The normal architecture of the spinal cord is radically disrupted by injury. After the initial insult, structure and function are lost through active secondary processes that involve reactive astrocytes, glial progenitors, microglia, macrophages, fibroblasts and Schwann cells. These cells produce chemokines and cytokines such as tumor necrosis factor (TNF)-α and interleukin (IL)-1β, which mediate the recruitment of inflammatory cells to the injury site. Targeting of these cytokines represents a potential strategy to reduce the secondary damage in SCI. In this review, we focus on several emerging strategies to neutralize TNF-α, including antibodies, soluble receptors, recombinant TNF-binding proteins, TNF receptor fusion proteins, and non-specific agents (e.g. thalidomide) and discuss their potential as therapy for SCI.
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