Direct In Vivo Evidence for α4-Integrin Mediated Interaction of Encephalitogenic T Cell Blasts with Endothelial VCAM-1 in the Spinal Cord White Matter Using Intravital Fluorescence Videomicroscopy
Until recently the central nervous system (CNS) has been considered to be an immunologically privileged site, where no immunosurveillance and hence no lymphocyte traffic occurs. This theory was supported by the fact that the CNS is able to exclude components of the immune system via the vascular blood-brain barrier (BBB) and lacks lymphatic drainage by classical lymphatic vessels. Thus, for many years there were few reasons for investigating lymphocyte traffic into the CNS. This situation has changed recently as it has become evident that during a wide range of inflammatory diseases of the CNS, mononuclear cells readily gain access to the CNS parenchyme, and that immunological mechanisms are intimately involved in the pathogenesis of these diseases. Because of its clinical and histopathological manifestations experimental autoimmune encephalomyelitis (EAE) is considered the best animal model for human T cell mediated inflammatory demyelinating diseases of the CNS such as multiple sclerosis (MS, Martin et al., 1992). In EAE autoaggressive CD4+ T cells gain access to the CNS parenchyme and cause inflammation, edema and demyelination within the CNS white matter.
KeywordsExperimental Autoimmune Encephalomyelitis Cell Blast Traffic Signal Transendothelial Migration Postcapillary Venule
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