Abstract
Multiple Sclerosis (MS) is a chronic demyelinating disease of the central nervous system (CNS) characterized by a multifocal inflammatory leukocyte infiltration and demyelination. It is widely accepted that an “activation” of CNS microvascular endothelial cells (EC) associated with blood-brain barrier (BBB) damage represents early event in demyelinating lesion development [1, 2]. However, the mechanisms responsible for the migration of lymphocytes through microvascular EC into the CNS have not been clearly identified. This traffic needs peripheral blood mononuclear cells (PBMC) activation, recruitment and strong adhesion to vascular ECs. Normally, vascular ECs have low adhesiveness for PBMC, but when stimulated by cytokines, such as interleukin-1, tumor necrosis factor and interferon gamma [3–5], released by inflammatory cells, they express surface adhesion proteins.
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© 1996 Springer-Verlag Italia, Milano
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Trojano, M., Avolio, C., Simone, I.L., Ruggieri, M., Livrea, P. (1996). Cerebrospinal fluid and serum soluble adhesion molecules in multiple sclerosis. In: Cerebrospinal Fluid Analysis in Multiple Sclerosis. Springer, Milano. https://doi.org/10.1007/978-88-470-2205-8_7
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DOI: https://doi.org/10.1007/978-88-470-2205-8_7
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