作者: S. LIGHTMAN , J. GREENWOOD
DOI: 10.1111/J.1365-2249.1992.TB06474.X
关键词: Blood–brain barrier 、 Blood–retinal barrier 、 Retina 、 Horseradish peroxidase 、 Pathology 、 Retinal 、 Immunology 、 Extravasation 、 Medicine 、 Infiltration (medical) 、 Tight junction
摘要: Using an experimental model of autoimmune uveoretinitis, we have examined the relationship T cell infiltration in retina to blood-retinal barrier (BRB) breakdown. Sensitive quantitative vivo techniques were used examine BRB permeability sucrose, a low mol. wt non-transported solute. Electron microscopy was also localize extravasated horseradish peroxidase, macromolecular visual tracer, from retinal vasculature and identify route by which any leakage occurring. No increase found prior lymphocytic infiltration. By day 10 disease inflammatory cells could be seen within structurally intact retina, shortly followed sucrose. Only later process, when damage photoreceptor layer became apparent, did extravasation macromolecule HRP occur. At no stage process there detectable inter-endothelial tight junctions. The size-dependancy tracer initial stages is indicative paracellular being responsible for permeability. In some evidence peroxidase filled 'vesicle-like' profiles observed. We suggest that devastating complication breakdown ocular inflammation direct consequence