Vascular cell adhesion molecule-1 modulation by tumor necrosis factor in experimental allergic encephalomyelitis.
Anti-tumor necrosis factor (TNF) antibodies inhibit passively transferred experimental allergic encephalomyelitis (EAE) in SJL mice. The possibility that this occurs through interference in TNF's upregulation of endothelial cell adhesion molecules was investigated. Expression of both vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) on spinal cord vessels increased during EAE. The upregulation of VCAM-1 was markedly reduced or prevented by anti-TNF treatment. Leukocytic infiltration was 15-fold lower in anti-TNF-treated than diseased animals. Spinal cord endothelial expression of VCAM-1, though not ICAM-1 or fibronectin, positively correlated with the extent of T cell, B cell or monocyte infiltration in each animal.
Barten
D M
DM
Department of Epidemiology and Public Health, Yale University School of Medicine, New Haven, CT 06520-8034.
Ruddle
N H
NH
D000818:Animals; D000911:Antibodies, Monoclonal / Q000627:therapeutic use*; D015815:Cell Adhesion Molecules / Q000032:analysis*; D002478:Cells, Cultured; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000473:pathology / Q000628:therapy*; D005260:Female; D005353:Fibronectins / Q000032:analysis; D006801:Humans; D007962:Leukocytes / Q000473:pathology; D051379:Mice; D016029:Receptors, Very Late Antigen / Q000032:analysis; D013116:Spinal Cord / Q000737:chemistry; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology*; D019010:Vascular Cell Adhesion Molecule-1
D000911:Antibodies, Monoclonal; D015815:Cell Adhesion Molecules; D005353:Fibronectins; D016029:Receptors, Very Late Antigen; D014409:Tumor Necrosis Factor-alpha; D019010:Vascular Cell Adhesion Molecule-1