ICAM-3 regulates lymphocyte morphology and integrin-mediated T cell interaction with endothelial cell and extracellular matrix ligands.

摘要: Leukocyte activation is a complex process that involves multiple cross-regulated cell adhesion events. In this report, we investigated the role of intercellular molecule-3 (ICAM-3), third identified ligand for beta 2 integrin leukocyte function-associated antigen-1 (LFA-1), in regulation to ICAM-1, vascular molecule-1 (VCAM-1), and 38- 80-kD fragments fibronectin (FN40 FN80). The activating anti-ICAM-3 HP2/19, but not other mAb, was able enhance T lymphoblast these proteins when combined with very low doses anti-CD3 which were unable by themselves induce phenomenon. contrast, anti-ICAM-1 mAb did attachment substrata. VCAM-1, FN40, FN80 specifically blocked anti-LFA-1, anti-VLA alpha 4, 5 respectively. HP2/19 also VLA-4- VLA-5-mediated binding leukemic Jurkat cells FN80, even absence cooccupancy CD3-TcR complex. We studied localization ICAM-3, LFA-1, VLA 1 integrin, immunofluorescence microscopy, on interacting VCAM-1 FN80. found promoted dramatic change morphology lymphoblasts allowed interact those ligands. Under conditions, it observed large contact area from an uropod-like structure (heading uropod) projected toward outer milieu. However, blasts stimulated promoting agents as TS2/16 or phorbol esters, detected. TP1/24 Notably, striking redistribution ICAM-3 induced agents. Thus, almost exclusively concentrated most distal portion heading uropod whereas either LFA-1 uniformly distributed all over area. Moreover, phenomenon TNF alpha-activated endothelial cells.(ABSTRACT TRUNCATED AT 400 WORDS)