Mechanisms That Regulate the Function of the Selectins and Their Ligands

TL;DR: The demonstration that selective modulation (blocking) of the adhesion molecule VLA-4 by natalizumab in MS, resembling that observed in experimental disease, represents a major advance in rational therapy.

TL;DR: Elevation of the levels of CECs, EMPS, EPCs, VEGF, and Ang-2 occurs during active vasculitis in children, and the levels declined with remission-inducing therapy in the individual patients.

TL;DR: A causal relationship between fucose treatment and selectin ligand expression and peripheral neutrophil counts is demonstrated, demonstrating that discontinuation of this therapy leads to the complete loss of E-selectin ligands within 3 days and of P-selectIn ligandsWithin 7 days.

TL;DR: It is demonstrated that CL-P1 predominantly mediated phagocytosis for fungi in vascular endothelia and real time reverse transcription-PCR analyses showed that other scavenger receptors, namely LOX-1, Stabilin-2, or macrophage receptor with collagenous structure, were not expressed in human umbilical vein endothelial cells isolated from different individuals.

TL;DR: Rolling of leukocytes on vascular endothelial cells, an early event in inflammation, can be reproduced in vitro on artificial lipid bilayers containing purified CD62, a selectin also named PADGEM and GMP-140 that is inducible on endothelial Cells.

TL;DR: Of considerable interest is the recent discovery that some chemokines function as HIV-suppressive factors by interacting with chemokine receptors which, together with CD4, were recognized as the binding sites for HIV-1.

TL;DR: Endothelial leukocyte adhesion molecule-1 (ELAM-1), a cell surface glycoprotein expressed by cytokine-activated endothelium, mediates the adhesion of blood neutrophils and may be a member of a nascent gene family of cell surface molecules involved in the regulation of inflammatory and immunological events at the interface of vessel wall and blood.