In neurodegenerative disorders, as well as in acute central nervous system (CNS) injuries, the initial impairment triggers a cascade of destructive events, collectively termed secondary degeneration, which eventually cause much more extensive damage. To investigate the process of secondary degeneration and ways to prevent it, we designed a well-calibrated model of optic nerve crush injury. Until recently, the main purpose of the immune system was thought to be protection of the body against alien pathogens. Since mechanical or biochemical insults do not involve exogenous pathogens, recruitment of the adaptive immune system was not considered relevant in such cases. We recently demonstrated, however, that a T-cell-mediated immune response directed against self-antigens residing in the site of damage can be beneficial for the injured optic nerve or spinal cord. This protective autoimmune response was found to be spontaneously evoked in some individuals, but not strongly enough to significantly affect recovery. Our aim was to boost this protective response in those individuals capable of spontaneously manifesting it, and to induce it in those incapable of manifesting it spontaneously. Optimal functional recovery requires the application of a proper combination of neuroprotection and neuroregeneration.