![]() Both Western blotting of circulating leukocytes from wild- type mice and fluorescence imaging of leukocyte- associated e. D confocal imaging was used to highlight CLN- 5 immunoreactivity in the central nervous system (CNS) and on leukocytes of mice with the neuroinflammatory condition experimental autoimmune encephalomyelitis (EAE). ![]() Given the expanding role of extracellular vesicles (EVs) in intercellular communication, we investigated whether EVs derived from brain microvascular endothelial cells (BMEC) of the BBB may play a role in transferring a major TJ protein, claudin- 5 (CLN- 5), to leukocytes as a possible basis for such a mechanism during neuroinflammation. Transient interactions between TJ proteins on the respective leukocyte and endothelial surfaces have been proposed as one mechanism for TEM. ![]() The mechanism of leukocyte transendothelial migration (TEM) across the highly restrictive blood- brain barrier (BBB) remains enigmatic, with paracellular TEM thought to require leukocytes to somehow navigate the obstructive endothelial tight junctions (TJs).
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