Expression of adhesion molecules and monocyte chemoattractant protein -1 (MCP-1) in the spinal cord lesions in HTLV-I-associated myelopathy.

Abstract:

:Leukocyte adhesion molecules to endothelium plays an important role in the pathogenesis of inflammatory diseases, including HTLV-I-associated myelopathy (HAM)/tropical spastic paraparesis (TSP). To help define the role of adhesion molecules in HAM/TSP, we studied the expression of lymphocyte function-associated antigen-1 (LFA-1), Mac-1, very late antigen-4 (VLA-4), Sialyl Lewisx (SLex), intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), endothelial leukocyte adhesion molecule-1 (ELAM-1) and monocyte chemoattractant protein-1 (MCP-1) in the spinal cord lesions of HAM/TSP. The results indicate that spinal cord lesions of HAM/TSP have greater VCAM-1 expression on endothelium compared with those of controls. Infiltrating mononuclear cells, especially perivascular lesions, expressed VLA-4. Although the expression of ICAM-1 in the spinal cords was not distinctive between HAM/TSP and controls, infiltrating mononuclear cells in the spinal cords of HAM/TSP strongly expressed LFA-1 and Mac-1. ELAM-1 was expressed on endothelium in the inactive-chronic lesions from three of five HAM/HAM/TSP, but was not detectable in the spinal cords of controls. SLex reactions was detectable on occasional perivascular cells in the spinal cord of HAM/TSP, but not in those controls. MCP-1 was detectable on perivascular infiltrating cells and vascular endothelium in active-chronic lesions. This study suggest that VLA-4/VCAM-1 interaction may play an important role for lymphocyte migration into the central nervous system (CNS) and MCP-1 may also be involved in inflammatory cell recruitment to the CNS in HAM/TSP.

journal_name

Acta Neuropathol

journal_title

Acta neuropathologica

authors

Umehara F,Izumo S,Takeya M,Takahashi K,Sato E,Osame M

doi

10.1007/s004010050435

subject

Has Abstract

pub_date

1996-01-01 00:00:00

pages

343-50

issue

4

eissn

0001-6322

issn

1432-0533

journal_volume

91

pub_type

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