The immune system has been found to be involved with positive and negative 
effects in the nervous system of amyotrophic lateral sclerosis (ALS) patients. 
In general, T cells, B cells, NK cells, mast cells, macrophages, dendritic 
cells, microglia, antibodies, complement and cytokines participate in limiting 
damage. Several mechanisms of action, such as production of neurotrophic growth 
factors and interaction with neurons and glial cells, have been shown to 
preserve these latter from injury and stimulate growth and repair. The immune 
system also participates in proliferation of neural progenitor stem cells and 
their migration to sites of injury and this activity has been documented in 
various neurologic disorders including traumatic injury, ischemic and 
hemorrhagic stroke, multiple sclerosis, infection, and neurodegenerative 
diseases (Alzheimer's disease, Parkinson's disease and ALS). Many therapies have 
been shown to stimulate the protective and regenerative aspects of the immune 
system in humans, such as intravenous immunoglobulins, and other experimental 
interventions such as vaccination, minocycline, antibodies and neural stem 
cells, have shown promise in animal models of ALS. Consequently, several 
immunosuppressive and immunomodulatory therapies have been tried in ALS, 
generally with no success, in particular intravenous immunoglobulins. The 
multiple aspects of the immune response in ALS are beginning to be appreciated, 
and their potential as pharmacologic targets in neurologic disease is being 
explored.