A monoclonal antibody to sialophorin (CD43) induces homotypic adhesion and activation of human monocytes

• Published in: The Journal of experimental medicine Vol. 170; no. 1; pp. 259 - 267
• Main Authors: YU-HUA NONG, REMOLD-O'DONNELL, E, LEBIEN, T. W, REMOLD, H. G
• Format: Journal Article
• Language: English
• Published: New York, NY Rockefeller University Press 01.07.1989; The Rockefeller University Press
• Subjects: Analysis of the immune response. Humoral and cellular immunity; Antibodies, Monoclonal - immunology; Antigen-Antibody Complex; Antigens, CD; Antigens, Differentiation - immunology; Biological and medical sciences; Calcium - pharmacology; Cell Adhesion - drug effects; Cell Aggregation - drug effects; Fundamental and applied biological sciences. Psychology; Fundamental immunology; Humans; Hydrogen Peroxide - blood; Immunobiology; Kinetics; Leukosialin; Magnesium - pharmacology; Monocytes - cytology; Monocytes - immunology; Monocytes - physiology; Organs and cells involved in the immune response; Sialoglycoproteins; Aggregation; Assay; Human; Monocyte; Activation; Monoclonal antibody; Macrophage aggregation test; Adhesion; Hydrogen Peroxides
• ISSN: 0022-1007; 1540-9538
• DOI: 10.1084/jem.170.1.259

Treatment of human monocytes for 24-48 h with the anti-CD43 mAb L10 caused five- to sevenfold stimulation of hydrogen peroxide-producing capacity, an established characteristic of activated monocytes. Peroxide-producing capacity induced by L10 antibody (1.6 +/- 0.3 nmol H2O2/micrograms DNA/h) was comparable with that induced by IFN-gamma (1.3 +/- 0.4 nmol H2O2/micrograms DNA/h), but appeared more rapidly (maximal at 24 h) than in the IFN-gamma-treated monocytes (maximal at 48 h). Treatment of monocytes with L10 mAb also caused dramatic increase in aggregation (homotypic adhesion). Induction of monocyte aggregation by L10 mAb required incubation for 1-8 h in the presence of Mg2+ and was abrogated by TA-1, an anti-LFA-1-alpha mAb. Thus, L10-induced monocyte activation proceeds via a Mg2+-requiring aggregation stage involving LFA-1. Whereas the extent of monocyte aggregation induced by L10 mAb and by IFN-gamma were comparable, the L10-induced aggregation occurred more rapidly (maximal at 8 h) than the IFN-gamma-induced aggregation (maximal at 24 h). The more rapid appearance of aggregation and increased hydrogen peroxide capacity in L10-treated monocytes suggests that the L10-induced activation pathway is independent of IFN-gamma-and IFN-gamma-R dependent events. These findings suggest that the surface molecule CD43 is the receptor of an independent activation pathway that leads in lymphocytes to proliferation and in monocytes to activation.