Inflammation is thought to exacerbate the outcome of spinal cord injury. However, our findings have led us to view inflammation as a healing response that needs the help of a systemic immune response mediated by T helper 1 (Th1) cells that are specific to the abundant antigens residing in the lesion site. Strains differ in their ability to manifest, at the right time and intensity, a spontaneous T-cell response to antigens at the lesion site and therefore in their ability to generate a local inflammatory response whose outcome is beneficial (maintenance and repair). All strains, however, can benefit from immune intervention that boosts and regulates the inflammatory response. Because recovery comprises multi-step processes, pharmacological intervention will be less effective than well-synchronized, self-healing immune activity. Risk-free neuroprotective intervention might be achieved by post-traumatic vaccination with a weak, non-pathogenic, auto-antigen, causing autoimmune T cells to home to the lesion site where they become activated and therefore activate local phagocytic cells to remove hostile elements and provide growth factors.