Normal EAE

aißi avßi a2ßiT a6ß1 avß3 a8ßi avßs aißi avßi a2ßiT a6ß1 avß3 a8ßi avßs

Figure 7.1 Expression of adhesion molecules and integrins on CNS endothelium and infiltrating immune cells in experimental autoimmune encephalomyelitis (EAE), and on glia in EAE. In rodent EAE, endothelial cells (E) of the CNS, infiltrating T-cells (T) and macrophages (Ma) have an adhesion molecule phenotype characteristic of a T-helper-1-mediated disease. Astrocytes (A) and oligodendrocytes (O) express a variety of integrins in normal rats. In acute EAE, there is an upregulation of the vitronectin and laminin receptors on astrocytes and neoexpression of a2p1 on oligodendrocytes, both mediated in vitro by tumor necrosis factor alpha (TNF-a), a central proinflammatory cytokine in EAE.


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