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

Gila Moalem, Raya Leibowitz-Amit, Eti Yoles, Felix Mor, Irun R. Cohen, Michal Schwartz*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review


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.

Original languageEnglish
Pages (from-to)49-55
Number of pages7
JournalNature Medicine
Issue number1
StatePublished - 1999
Externally publishedYes


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