Figure 2.

PMN adhesion and transendothelial migration (TEM). (A) Resting PMNs express beta-2 (β₂) integrins and selectin ligands, but unstimulated endothelial cells (ECs) do not express selectins and are, thus, unable to bind circulating PMNs. (B) Microbial infections and proinflammatory mediators stimulate the endothelium, and activated ECs express cell surface adhesion molecules (P-selectin, E-selectin, and intercellular adhesion molecule-1 (ICAM-1)), which interact with their counter receptors on PMNs. Primary PMN capture and secondary PMN–PMN tethering are facilitated by interactions between selectins and selectin ligands. As captured PMNs slow in circulation and roll along the endothelium, β₂ integrins are activated. (C) Activated β₂ integrins interact with EC ICAM-1, which clusters to promote firm EC-PMN adhesion. β₂-integrin/ICAM-1 interaction facilitates PMN spreading and crawling, and eventually, PMN transendothelial migration.