Soon after the mechanical injury, monocytes infiltrate into the spinal cord and differentiate into macrophages. Activated resident microglia and macrophages also secrete numerous cytokines, free radicals, and growth factors, which, in turn, affect
nearby cells in positive and negative ways (Lindholm et al.1992, Schnell et al. 1999, Anderson 2002). The growth factors are critical for neuron survival and tissue
repair. However, free radicals and pro-inflammatory cytokines contribute to expansion of the lesion, worsening the impact of the injury. The role of lymphocytes
in spinal cord injuries is rather controversial. Some argue that one type of lymphocyte (autoreactive T-lymphocytes) have destructive properties: according to this schema they exacerbate injury to axons and induce demyelination, leading to functional loss
(Popovich and Jones 2003). Others argue that this lymphocyte is not pathological but, rather, confers protection to the myelin-insulated neurons (Schwartz and Kipnis 2001, Kipnis et al. 2002). Protection of myelin also protects the integrity of the axon that it insulates. To summarize, the exacerbating effect of the uncontrolled immune system on the injured spinal cord is to a large extent both inflammatory and free radical
mediated. The immune system would only be of net benefit if exogenously controlled.