The limitation of immune responsiveness in the mammalian CNS has been attributed to the intricate nature of neuronal networks, which would appear to be more susceptible than other tissues to the threat of permanent disorganization when exposed to massive inflammation. This line of logic led to the conclusion that all forms of CNS inflammation would do more harm than good and, hence, the less immune intervention the better. However, mounting evidence indicates that some forms of immune-system intervention can help to protect or restore CNS integrity. We have shown that the innate immune system, represented by activated macrophages, can facilitate the processes of regeneration in the severed spinal cord. More recently, we found that autoimmune T cells that are specific for a component of myelin can protect CNS neurons from the catastrophic secondary degeneration, which extends traumatic lesions to adjacent CNS areas that did not suffer direct damage. The challenge, therefore, is to learn how to modify immune interactions in the traumatized CNS in order to promote its post-injury maintenance and repair.