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

Nat Med. 1999 Jan;5(1):49-55. doi: 10.1038/4734.


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.

MeSH terms

  • Amino Acid Sequence
  • Animals
  • Autoimmunity / immunology*
  • Axotomy
  • Central Nervous System / immunology
  • Central Nervous System / surgery
  • Female
  • Molecular Sequence Data
  • Myelin Basic Protein / immunology
  • Nerve Degeneration / prevention & control*
  • Neurons*
  • Optic Nerve / cytology
  • Optic Nerve Injuries*
  • Rats
  • Rats, Inbred Lew
  • T-Lymphocytes / immunology*


  • Myelin Basic Protein