Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0276640 (TEM)
 20,729 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To help assess the immunological functions of the liver peritoneum, expression and 3D-microlocalization of adhesion molecules were studied by immuno-SEM and -TEM. The peritoneal tissues of the liver obtained from lipopolysaccharide (LPS, 1.5 microg/g BW for 24 hr)-stimulated (n = 18 including nine controls) and non-stimulated mice (n = 6 including three controls) were analyzed by immunolabeling with 15 nm gold particle single-labeling analysis of ICAM-1, ICAM-2, VCAM-1, MAdCAM-1, PECAM-1, ELAM-1, and CD105 expression. In addition, 10 and 20 nm gold particle double-labeling analysis of ICAM-1 and VCAM-1 was carried out with conventional TEM and BSE (backscatter electron) imaging. Gold particles detected in the peritoneal mesothelial cells were quantified using a computer analyzer, LUZEX III. Only ICAM-1 in non-stimulated mice and both ICAM-1 and VCAM-1 in LPS-stimulated mice were expressed on the mesothelium, but no other adhesion molecules were detected in either condition. Expression of ICAM-1 was consistently about four times greater than that of VCAM-1. Each adhesion molecule was restricted to the microvilli. ICAM-1 was expressed on all microvilli and tended to form clusters of three or four molecules. On the other hand, about 24% of the microvilli expressed VCAM-1 and less clustering was seen. Double-labeling techniques disclosed that VCAM-1 and ICAM-1 were rarely closely associated, usually spaced by about 40 nm. These results suggest that microvilli of the mesothelial cell play a significant role in leukocyte migration in the peritoneal cavity, by providing the important substrates for adhesion, ICAM-1 and VCAM-1.
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PMID:Expression of adhesion molecules relevant to leukocyte migration on the microvilli of liver peritoneal mesothelial cells. 1060 47

The extravasation of CD4(+) effector/memory T cells (TEM cells) across the blood-brain barrier (BBB) is a crucial step in the pathogenesis of experimental autoimmune encephalomyelitis (EAE) or multiple sclerosis (MS). Endothelial ICAM-1 and ICAM-2 are essential for CD4(+) TEM cell crawling on the BBB prior to diapedesis. Here, we investigated the influence of cell surface levels of endothelial ICAM-1 in determining the cellular route of CD4(+) TEM -cell diapedesis across cytokine treated primary mouse BBB endothelial cells under physiological flow. Inflammatory conditions, inducing high levels of endothelial ICAM-1, promoted rapid initiation of transcellular diapedesis of CD4(+) T cells across the BBB, while intermediate levels of endothelial ICAM-1 favored paracellular CD4(+) T-cell diapedesis. Importantly, the route of T-cell diapedesis across the BBB was independent of loss of BBB barrier properties. Unexpectedly, a low number of CD4(+) TEM cells was found to cross the inflamed BBB in the absence of endothelial ICAM-1 and ICAM-2 via an obviously alternatively regulated transcellular pathway. In vivo, this translated to the development of ameliorated EAE in ICAM-1(null) //ICAM-2(-/-) C57BL/6J mice. Taken together, our study demonstrates that cell surface levels of endothelial ICAM-1 rather than the inflammatory stimulus or BBB integrity influence the pathway of T-cell diapedesis across the BBB.
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PMID:Cell surface levels of endothelial ICAM-1 influence the transcellular or paracellular T-cell diapedesis across the blood-brain barrier. 2554 37