PMID: 7542307Jul 1, 1995Paper

IL-1 activation of endothelium supports VLA-4 (CD49d/CD29)-mediated monocyte transendothelial migration to C5a, MIP-1 alpha, RANTES, and PAF but inhibits migration to MCP-1: a regulatory role for endothelium-derived MCP-1

Journal of Leukocyte Biology
H E ChuluyanA C Issekutz

Abstract

We investigated the effect of interleukin-1 (IL-1) activation of human umbilical vein endothelium (HUVE) on human monocyte transendothelial migration induced by chemotactic factors. Monocyte migration across unactivated endothelium in response to macrophage inflammatory protein-1 alpha (MIP-1 alpha), RANTES, platelet-activating factor (PAF), or monocyte chemoattractant protein-1 (MCP-1) was completely inhibited (90%) by monoclonal antibodies (mAbs; 60.3) to CD18 of the CD11/CD18 complex on the monocyte and partially inhibited (by 75%) in response to C5a. When the HUVE was stimulated with IL-1 alpha (5 h, 0.1 ng/ml), monocyte migration in response to C5a, MIP-1 alpha, RANTES, or PAF was no longer inhibited by mAb to CD18. However, migration was blocked by the combination of mAb to the alpha 4-integrin (CD49d) chain of very late antigen-4 (CD49d/CD29) with the mAb to CD18. In contrast to the above stimuli, activation of the HUVE with IL-1 alpha inhibited the transendothelial migration of monocytes in response to MCP-1. mAbs to the adhesion molecules up-regulated on HUVE by IL-1, i.e., E-selectin (CD62E), intercellular adhesion molecule-1 (CD54) or vascular cell adhesion molecule-1 (CD106), did not reverse the inhibitory effect. T...Continue Reading

Citations

Oct 18, 2000·Journal of Neurochemistry·A V Andjelkovic, J S Pachter
Oct 22, 2003·The Journal of Immunology : Official Journal of the American Association of Immunologists·Konstantin MayerWerner Seeger
Nov 13, 2004·Journal of Bone and Mineral Research : the Official Journal of the American Society for Bone and Mineral Research·Xuefeng YuPhilip Osdoby
Jan 6, 2007·Circulation Research·Philipp von Hundelshausen, Christian Weber
Mar 17, 2010·The Journal of Immunology : Official Journal of the American Association of Immunologists·Shiva ShahraraRichard M Pope
Sep 22, 1998·Scandinavian Journal of Immunology·P StohlawetzP Pietschmann
Sep 25, 2003·Physiological Reviews·Bjarne Osterud, Eirik Bjorklid
May 17, 2017·Alzheimer's & Dementia : Diagnosis, Assessment & Disease Monitoring·Veer Bala GuptaUNKNOWN AIBL Research Group
Nov 1, 1996·Journal of Clinical Immunology·T Uchiyama
Jul 19, 2002·American Journal of Physiology. Heart and Circulatory Physiology·Konstantin MayerWerner Seeger
Feb 21, 2016·The Journal of Biological Chemistry·Wulin AerbajinaiGriffin P Rodgers
Jun 11, 2002·The Journal of Immunology : Official Journal of the American Association of Immunologists·Karkada MohanThomas B Issekutz
Jan 8, 1999·The Journal of Surgical Research·I D McGilvrayO D Rotstein
Dec 1, 1996·Cytokine & Growth Factor Reviews·D D Taub
Oct 26, 1999·Cellular Signalling·G Berton, C A Lowell

❮ Previous
Next ❯

Related Concepts

Related Feeds

Alternative Complement Pathway

The Alternative Complement Pathway is part of the innate immune system, and activation generates membrane attack complexes that kill pathogenic cells. Discover the latest research on the Alternative Complement Pathway.

Adhesion Molecules in Health and Disease

Cell adhesion molecules are a subset of cell adhesion proteins located on the cell surface involved in binding with other cells or with the extracellular matrix in the process called cell adhesion. In essence, cell adhesion molecules help cells stick to each other and to their surroundings. Cell adhesion is a crucial component in maintaining tissue structure and function. Discover the latest research on adhesion molecule and their role in health and disease here.