TY - JOUR
T1 - Enhancement of human monocyte cytotoxicity by both interferon-γ and -β and comparison to other stimuli
AU - Sharon, Nechema
AU - Shoham, J.
AU - Passwell, J. H.
PY - 1989
Y1 - 1989
N2 - Recombinant interferon preparations caused a dose-dependent increase of human monocyte cytotoxicity to the K562 and Daudi cell lines. Both rIFN-γ and rIFN-β enhanced this function to a similar extent, while rIFN-αc had less effect when compared on the basis of their anti-viral effects. Endotoxin and concanavalin A increased basal monocyte cytotoxicity while phagocytosis of latex particles had no effect. The increased monocyte cytotoxic effect of rIFN-β was completely abrogated by monoclonal antibody to IFN-β, while monoclonal antibody to IFN-γ had no effect. However, monoclonal antibody to IFN-γ only reduced the increased cytotoxic effect caused by rIFN-γ by 25%. Catalase inhibited both basal monocyte cytotoxicity and the increase in cytotoxicity following addition of rIFN-γ only slightly, suggesting that mechanisms other than the oxidative burst were active and could be induced by rIFN-γ.
AB - Recombinant interferon preparations caused a dose-dependent increase of human monocyte cytotoxicity to the K562 and Daudi cell lines. Both rIFN-γ and rIFN-β enhanced this function to a similar extent, while rIFN-αc had less effect when compared on the basis of their anti-viral effects. Endotoxin and concanavalin A increased basal monocyte cytotoxicity while phagocytosis of latex particles had no effect. The increased monocyte cytotoxic effect of rIFN-β was completely abrogated by monoclonal antibody to IFN-β, while monoclonal antibody to IFN-γ had no effect. However, monoclonal antibody to IFN-γ only reduced the increased cytotoxic effect caused by rIFN-γ by 25%. Catalase inhibited both basal monocyte cytotoxicity and the increase in cytotoxicity following addition of rIFN-γ only slightly, suggesting that mechanisms other than the oxidative burst were active and could be induced by rIFN-γ.
UR - http://www.scopus.com/inward/record.url?scp=0024456465&partnerID=8YFLogxK
U2 - 10.1016/0192-0561(89)90128-8
DO - 10.1016/0192-0561(89)90128-8
M3 - ???researchoutput.researchoutputtypes.contributiontojournal.article???
C2 - 2513281
AN - SCOPUS:0024456465
SN - 0192-0561
VL - 11
SP - 743
EP - 749
JO - International Journal of Immunopharmacology
JF - International Journal of Immunopharmacology
IS - 7
ER -