Autoimmunity to antigens of the central nervous system is usually considered
detrimental. T cells specific to a central nervous system self antigen, such
as myelin basic protein, can indeed induce experimental autoimmune encephalomyelitis,
but such T cells may nevertheless appear in the blood of healthy individuals.
We show here that autoimmune T cells specific to myelin basic protein can
protect injured central nervous system neurons from secondary degeneration.
After a partial crush injury of the optic nerve, rats injected with activated
anti−myelin basic protein T cells retained approximately 300% more retinal
ganglion cells with functionally intact axons than did rats injected with
activated T cells specific for other antigens. Electrophysiological analysis
confirmed this finding and suggested that the neuroprotection could result
from a transient reduction in energy requirements owing to a transient reduction
in nerve activity. These findings indicate that T−cell autoimmunity
in the central nervous system, under certain circumstances, can exert a beneficial
effect by protecting injured neurons from the spread of damage.
