CROSS-LINKING OF ICAM-1 INDUCES COSIGNALING OF AN OXIDATIVE BURST FROM MONONUCLEAR LEUKOCYTES

Citation
R. Rothlein et al., CROSS-LINKING OF ICAM-1 INDUCES COSIGNALING OF AN OXIDATIVE BURST FROM MONONUCLEAR LEUKOCYTES, The Journal of immunology, 152(5), 1994, pp. 2488-2495
Citations number
49
Categorie Soggetti
Immunology
Journal title
The Journal of immunology
ISSN journal
00221767 → ACNP
Volume
152
Issue
5
Year of publication
1994
Pages
2488 - 2495
Database
ISI
SICI code
0022-1767(1994)152:5<2488:COIICO>2.0.ZU;2-S
Abstract
Cell adhesion molecules were first described as accessory molecules si mply to bridge one cell to another. More recently, it has been realize d that these molecules also transmit signals from outside of the cell to inside. We show that cross-linking of the ICAM-1 on the cell membra ne with anti-ICAM-1 mAb and F(ab')(2) fragments of goat anti-MlgG in t he presence of suboptimal levels of the bacterial peptide FMLP results in co-stimulation of an oxidative burst from CD14 expressing PBMCs. T he amplitude of the oxidative response was less than the oxidative bur st induced by CD18 cross-linking, whereas the response was more prolon ged. On the other hand, cross-linking by anti-L-selectin mAb plus F(ab ')(2) fragments of goat anti-MlgG induced a minimal oxidative burst th at was not significantly greater than the response generated by anti-L -selectin mAb alone. The addition of an excess of soluble ICAM-1 to co mpete for the anti-ICAM-1 mAb inhibits the oxidative burst in response to ICAM-1 cross-linking but not to CD18 cross-linking. These results suggest that ICAM-1 is capable of delivering a transmembrane signal in to CD14-positive PBMC.