Autoimmune T cells protect neurons from secondary degeneration after central nervous system axotomy

Autoimmunity to antigens of the central nervous system is usually considere d detrimental. T cells specific to a central nervous system self antigen, s uch as myelin basic protein, can indeed induce experimental autoimmune ence phalomyelitis, but such T cells may nevertheless appear in the blood of hea lthy individuals. We show here that autoimmune T cells specific to myelin b asic protein can protect injured central nervous system neurons from second ary degeneration. After a partial crush injury of the optic nerve, rats inj ected with activated anti-myelin basic protein T cells retained approximate ly 300% more retinal ganglion cells with functionally intact axons than did rats injected with activated T cells specific for other antigens. Electrop hysiological analysis confirmed this finding and suggested that the neuropr otection could result from a transient reduction in energy requirements owi ng to a transient reduction in nerve activity. These findings indicate that T-cell autoimmunity in the central nervous system, under certain circumsta nces, can exert a beneficial effect by protecting injured neurons from the spread of damage.