While some aspects of the inflammatory and immunologic response mediated by these cytokines may be beneficial after spinal cord injury, others may be detrimental. (Bethea, 2000) For example, after a contusion spinal cord injury, transgenic mice lacking the TNF receptor were found to have increased apoptosis, a larger area of secondary injury, and worse locomotor scores than wild-type mice. (Kim et al., 2001) Conversely, the systemic administration of IL-10 significantly reduced neuronal damage after an excitotoxic spinal cord injury. (Brewer et al., 1999) A more sophisticated understanding of these complex responses is obviously needed. Nevertheless, these animal studies demonstrate the proof of concept that the manipulation of these cytokine responses has the potential to influence outcome after spinal cord injury, and therefore, may represent the targets for neuroprotective intervention. The levels of expression for each cytokine appear to change over time and the temporal specificity of the expression likely also influences the inflammatory response.