Effects of autoimmunity on recovery of function in adult rats following spinal cord injury

He Zuo Lü, Liang Xu, Jian Zou, Yan Xia Wang, Zheng Wen Ma, Xiao Ming Xu, Pei Hua Lu

Research output: Contribution to journalArticlepeer-review

32 Scopus citations


The central nervous system (CNS) is considered to be an immune-privileged site. For a long time, autoimmunity-induced inflammation has been viewed as an important mediator of secondary damage in the CNS following injury. However, other studies also suggest that autoimmunity is protective and beneficial. To investigate whether protective autoimmunity is present following spinal cord injury (SCI), we employed neonatally thymectomized (Tx) rats which contain few T lymphocytes in their peripheral blood, and passively immunized them with T lymphocytes activated by myelin basic protein (MBP) or spinal cord homogenate (SCH). Here we report that, among Tx, sham-Tx (sTx) and normal rats that received a contusive SCI, no significant histological and behavioral differences were found, suggesting that the endogenous T lymphocytes had no significant influence on the pathogenesis of secondary SCI. In rats passively immunized with MBP- or SCH-activated T cells (MBP-T or SCH-T, respectively), similar numbers of CD4+ T cells were found to infiltrate into the injured spinal cords. However, only the MBP-T immunization showed neuroprotection, evidenced by the reduction of post-traumatic neuronal losses and improvement of functional recovery. These results collectively suggest that not all T lymphocytes against CNS antigens are neuroprotective and that a subpopulation of them, such as those of MBP-T cells, could be beneficial for SCI repair.

Original languageEnglish (US)
Pages (from-to)1217-1230
Number of pages14
JournalBrain, Behavior, and Immunity
Issue number8
StatePublished - Nov 2008


  • Autoimmunity
  • Myelin basic protein
  • Neuroprotection
  • Passive immunization
  • Spinal cord injury
  • Thymectomy

ASJC Scopus subject areas

  • Immunology
  • Behavioral Neuroscience
  • Endocrine and Autonomic Systems

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