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

J Neuroimmunol. 2004 Jan;146(1-2):94-8. doi: 10.1016/j.jneuroim.2003.10.055.

Abstract

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.

Publication types

  • Comparative Study
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Antigens, CD / biosynthesis
  • Antigens, CD / physiology*
  • B7-1 Antigen / biosynthesis
  • B7-1 Antigen / physiology*
  • B7-2 Antigen
  • Membrane Glycoproteins / biosynthesis
  • Membrane Glycoproteins / physiology*
  • Pain Measurement / methods
  • Peripheral Nervous System Diseases / immunology
  • Peripheral Nervous System Diseases / metabolism*
  • Rats
  • Spinal Cord / immunology
  • Spinal Cord / metabolism
  • Spinal Nerves / immunology
  • Spinal Nerves / metabolism*
  • Spinal Nerves / pathology*

Substances

  • Antigens, CD
  • B7-1 Antigen
  • B7-2 Antigen
  • Cd86 protein, rat
  • Membrane Glycoproteins