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The Journal of Neuroscience, July 13, 2005, 25(28):6576-6583; doi:10.1523/JNEUROSCI.0305-05.2005

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Development/Plasticity/Repair
Molecular Control of Physiological and Pathological T-Cell Recruitment after Mouse Spinal Cord Injury

T. Bucky Jones,^1,4 Ronald P. Hart,⁵ and Phillip G. Popovich^1,2,3,4

¹The Neuroscience Graduate Studies Program, ²Department of Molecular Virology, Immunology, and Medical Genetics, ³The Institute for Behavioral Medicine Research, and ⁴The Spinal Trauma and Repair Laboratories, The Ohio State University College of Medicine and Public Health, Columbus, Ohio 43210, and ⁵W. M. Keck Center for Collaborative Neuroscience, Rutgers University, Piscataway, New Jersey 08854

The intraspinal cues that orchestrate T-cell migration and activation after spinal contusion injury were characterized using B10.PL (wild-type) and transgenic (Tg) mice with a T-cell repertoire biased toward recognition of myelin basic protein (MBP). Previously, we showed that these strains exhibit distinct anatomical and behavioral phenotypes. In Tg mice, MBP-reactive T-cells are activated by spinal cord injury (SCI), causing more severe axonal injury, demyelination, and functional impairment than is found in non-Tg wild-type mice (B10.PL). Conversely, despite a robust SCI-induced T-cell response in B10.PL mice, no overt T-cell-mediated pathology was evident. Here, we show that chronic intraspinal T-cell accumulation in B10.PL and Tg mice is associated with a dramatic and sustained increase in CXCL10/IP-10 and CCL5/RANTES mRNA expression. However, in Tg mice, chemokine mRNA were enhanced 2- to 17-fold higher than in B10.PL mice and were associated with accelerated intraspinal T-cell influx and enhanced CNS macrophage activation throughout the spinal cord. These data suggest common molecular pathways for initiating T-cell responses after SCI in mice; however, if T-cell reactions are biased against MBP, molecular and cellular determinants of neuroinflammation are magnified in parallel with exacerbation of neuropathology and functional impairment.

Key words: macrophage; microglia; neuroinflammation; spinal cord injury; T-lymphocyte; chemokines; myelin basic protein

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Received Jan 21, 2005; revised May 31, 2005; accepted June 1, 2005.

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