PMID- 8928610
OWN - NLM
STAT- MEDLINE
DCOM- 19961127
LR  - 20190812
IS  - 0001-6322 (Print)
IS  - 0001-6322 (Linking)
VI  - 91
IP  - 4
DP  - 1996
TI  - Expression of adhesion molecules and monocyte chemoattractant protein -1 (MCP-1) 
      in the spinal cord lesions in HTLV-I-associated myelopathy.
PG  - 343-50
AB  - 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.
FAU - Umehara, F
AU  - Umehara F
AD  - Third Department of Internal Medicine, Kagoshima University School of Medicine, 
      Japan.
FAU - Izumo, S
AU  - Izumo S
FAU - Takeya, M
AU  - Takeya M
FAU - Takahashi, K
AU  - Takahashi K
FAU - Sato, E
AU  - Sato E
FAU - Osame, M
AU  - Osame M
LA  - eng
PT  - Journal Article
PL  - Germany
TA  - Acta Neuropathol
JT  - Acta neuropathologica
JID - 0412041
RN  - 0 (Chemokine CCL2)
RN  - 0 (Vascular Cell Adhesion Molecule-1)
SB  - IM
MH  - Aged
MH  - Chemokine CCL2/*metabolism
MH  - Female
MH  - Humans
MH  - Immunohistochemistry
MH  - Male
MH  - Middle Aged
MH  - Spinal Cord Injuries/*metabolism
MH  - Vascular Cell Adhesion Molecule-1/*metabolism
EDAT- 1996/01/01 00:00
MHDA- 1996/01/01 00:01
CRDT- 1996/01/01 00:00
PHST- 1996/01/01 00:00 [pubmed]
PHST- 1996/01/01 00:01 [medline]
PHST- 1996/01/01 00:00 [entrez]
AID - 10.1007/s004010050435 [doi]
PST - ppublish
SO  - Acta Neuropathol. 1996;91(4):343-50. doi: 10.1007/s004010050435.