Fig. 4.

Teff and Treg immunity in ALS and stroke. In ALS, Teffs perpetrate innate microglial inflammation by misfolded SOD inciting oxidative stress and affecting astrocyte function linked to glutamate uptake, ensuring motor neuronal cell death with the primary clinical manifestations of disease. Parallel responses are operative in Stroke. Following ischemic stroke, peripheral Teffs accumulate at the brain injury site to participate in local inflammatory responses manifested by micro- and astrogliosis and secondary neuronal injuries. Following acute episode, injuries are contained, in part, through the emergence of Tregs that serve to reduce astrogliosis, promote synapse formation, and decrease the extent of injury. Tregs are neuroprotective mediators in each of these pathological processes and herald slow disease progression and control of neurodegenerative activities