Expression of adhesion molecules and histocompatibility antigens at the blood-brain barrier.
The migration of inflammatory cells through the blood-brain barrier in health and disease involves complex interactions between hematogenous cells, endothelial cells, the basement membrane and the perivascular glia limitans. Recent evidence is presented, suggesting that part of these interactions involve antigen independent mechanisms, mediated by cellular adhesion molecules. The accessibility of endothelial adhesion molecules in the intact blood-brain barrier is lower compared to vessels in other organs. This may account for the low traffic of hematogenous cells through the normal blood-brain barrier. However, in inflammatory conditions the expression of endothelial adhesion molecules is upregulated, which may lead to recruitment of inflammatory cells into the lesions. Antigen specific activation of T-cells at the blood-brain barrier apparently takes place mainly at perivascular monocytes and microglia cells. In severe inflammatory lesions, however, astrocytes may be additionally involved in antigen presentation.
Lassmann
H
H
Research Unit for Experimental Neuropathology, Austrian Academy of Sciences, University of Vienna.
Rössler
K
K
Zimprich
F
F
Vass
K
K
D000818:Animals; D000938:Antigen-Presenting Cells; D000941:Antigens / Q000276:immunology; D001812:Blood-Brain Barrier; D015815:Cell Adhesion Molecules / Q000096:biosynthesis* / Q000235:genetics; D002465:Cell Movement; D002493:Central Nervous System Diseases / Q000378:metabolism / Q000473:pathology; D016207:Cytokines / Q000502:physiology; D004730:Endothelium, Vascular / Q000378:metabolism; D005786:Gene Expression Regulation; D006649:Histocompatibility Antigens / Q000096:biosynthesis* / Q000235:genetics; D006801:Humans; D007249:Inflammation; D007962:Leukocytes / Q000378:metabolism; D008213:Lymphocyte Activation; D016176:T-Lymphocyte Subsets / Q000276:immunology
D000941:Antigens; D015815:Cell Adhesion Molecules; D016207:Cytokines; D006649:Histocompatibility Antigens