Increased ICAM-1 and VCAM-1 expression in the brains of autoimmune mice.
Pathogenic mechanisms of central nervous system (CNS) involvement in systemic lupus erythematosus (SLE) remain unknown. We recently reported the presence of autoantibodies in the brain tissue ex vivo of autoimmune MRL/lpr mice. We postulated that at least some of these autoantibodies are produced in situ because of B-cell entry into the brain. The blood-brain barrier (BBB) blocks the entry of most large molecules and cells into the brain. In certain CNS pathologies, however, immune cells gain entry due to elevated expression of adhesion molecules. This study looked at adhesion molecule expression, ICAM-1 and VCAM-1, in the brains of MRL/lpr mice. Using immunofluorescent antibody binding assays and confocal laser imaging, we show that expression of ICAM-1 and VCAM-1 is elevated in MRL/lpr mice brains at 4 months of age as compared to age-matched controls. These results suggest a possible mechanism for leukocyte entry into the brains of autoimmune mice that in turn suggest immune-mediated pathology in CNS-lupus.
D000818:Animals; D001921:Brain / Q000276:immunology* / Q000378:metabolism* / Q000473:pathology; D002552:Cerebral Ventricles / Q000737:chemistry / Q000276:immunology / Q000473:pathology; D002831:Choroid Plexus / Q000737:chemistry / Q000276:immunology / Q000473:pathology; D004730:Endothelium, Vascular / Q000737:chemistry / Q000276:immunology / Q000473:pathology; D004797:Enzyme-Linked Immunosorbent Assay; D018799:Intercellular Adhesion Molecule-1 / Q000032:analysis / Q000096:biosynthesis*; D008180:Lupus Erythematosus, Systemic / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D051379:Mice; D020297:Mice, Congenic; D008810:Mice, Inbred C57BL; D019463:Mice, Inbred MRL lpr; D015854:Up-Regulation / Q000276:immunology*; D019010:Vascular Cell Adhesion Molecule-1 / Q000032:analysis / Q000096:biosynthesis*
D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1