Presence of spinal B7.2 (CD86) but not B7.1 (CD80) co-stimulatory molecules following peripheral nerve injury: role of nondestructive immunity in neuropathic pain.

Previous work in our laboratory demonstrated spinal neuroimmune activation and leukocyte trafficking into the central nervous system (CNS) parenchyma in a rat model of neuropathic pain. Recent studies suggest that co-stimulatory molecules B7.1 (CD80) and B7.2 (CD86) play a differential role in the effect of beneficial versus deleterious CNS autoimmune responses. In the present study, we determined the lumbar spinal expression of the co-stimulatory molecules B7.1 and B7.2 in a rat model of neuropathy. We observed intense B7.2 microglial immunoreactivity in the lumbar spinal cord following the injury but no expression of B7.1. These data suggest a role of protective CNS autoimmunity following peripheral nerve injury.