High-mannose intercellular adhesion molecule-1 (ICAM-1) enhances CD16+ monocyte adhesion to the endothelium.

High-mannose intercellular adhesion molecule-1 (ICAM-1) enhances CD16+ monocyte adhesion to the endothelium.
Am J Physiol Heart Circ Physiol. 2019 Aug 09;:
Authors: Regal-McDonald K, Xu B, Barnes JW, Patel RP
Abstract
Human monocytes have been classified into three distinct groups - classical (anti-inflammatory; CD14+/CD16-), non-classical (patrolling; CD14+/CD16++), and intermediate (pro-inflammatory; CD14++/CD16+). Adhesion of non-classical / intermediate monocytes with the endothelium is important for innate immunity, and also vascular inflammatory disease. However, there is an incomplete understanding of the mechanisms that regulate CD16+ vs. CD16- monocyte adhesion to the inflamed endothelium. Here, we tested the hypothesis that a high mannose (HM) N-glycoform of intercellular adhesion molecule-1 (ICAM-1) on the endothelium mediates the selective recruitment of CD16+ monocytes. Using TNFα treatment of human umbilical vein endothelial cells (HUVECs), and using proximity ligation assay (PLA) for detecting proximity of specific N-glycans and ICAM-1, we show that TNFa induces HM-ICAM-1 formation on the endothelial surface in a time-dependent manner. Next, we measured CD16- or CD16+ monocyte rolling and adhesion to TNFα treated HUVECs in which HM- or hybrid ICAM-1 N-glycoforms were generated using the a-mannosidase class I and II inhibitors, Kifunensine and Swainsonine, respectively. Expression of HM-ICAM-1 selectively enhanced CD1...

Source: American Journal of Physiology. Heart and Circulatory Physiology - August 8, 2019 Category: Physiology Authors: Regal-McDonald K, Xu B, Barnes JW, Patel RP Tags: Am J Physiol Heart Circ Physiol Source Type: research