TY - JOUR
T1 - Effect of α1-acidic glycoprotein in the ascitic fluid of cancer patients on human NK cells
T2 - Selective suppression of interferon-induced NK activation
AU - Aso, Hisashi
AU - Tamura, Keiji
AU - Rose, Michael T.
AU - Tomioka, Yoshihisa
AU - Mizugaki, Michinao
AU - Ishida, Nakao
PY - 1999/1/1
Y1 - 1999/1/1
N2 - The in vitro effect of C-AGP (pure α1-acid glycoprotein from the ascitic fluid of cancer patients) on NK cell cytotoxicity was tested using normal healthy human PBMC. C-AGP had no inhibitory effect on basal NK cell activity. C-AGP selectively suppressed the augmentation of NR cell activity by rIFNαA and rIFNγ, but C-AGP did not prevent the NK activation by rIL-2. NK cells in PBMC treated with C-AGP for 12 h and then washed just once, to remove the C-AGP, fully recovered the ability to respond to rIFNαA. However, after the treatment of PBMC with C-AGP for 5 or 6 days, NK cells failed to respond to rIFNαA, in spite of washing to remove C-AGP from the cultures. Monocytes were necessary for the suppressive effect of C-AGP on rIFNαA activation of NK cells. Indomethacin restored the ability of NK cells to respond to rIFN(yA in C-AGP treated PBMC. These results suggest that monocytes are able to selectively suppress the response of NK cells to IFNs in the presence of, or following treatment with C-AGP.
AB - The in vitro effect of C-AGP (pure α1-acid glycoprotein from the ascitic fluid of cancer patients) on NK cell cytotoxicity was tested using normal healthy human PBMC. C-AGP had no inhibitory effect on basal NK cell activity. C-AGP selectively suppressed the augmentation of NR cell activity by rIFNαA and rIFNγ, but C-AGP did not prevent the NK activation by rIL-2. NK cells in PBMC treated with C-AGP for 12 h and then washed just once, to remove the C-AGP, fully recovered the ability to respond to rIFNαA. However, after the treatment of PBMC with C-AGP for 5 or 6 days, NK cells failed to respond to rIFNαA, in spite of washing to remove C-AGP from the cultures. Monocytes were necessary for the suppressive effect of C-AGP on rIFNαA activation of NK cells. Indomethacin restored the ability of NK cells to respond to rIFN(yA in C-AGP treated PBMC. These results suggest that monocytes are able to selectively suppress the response of NK cells to IFNs in the presence of, or following treatment with C-AGP.
UR - http://www.scopus.com/inward/record.url?scp=0032896798&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0032896798&partnerID=8YFLogxK
U2 - 10.1023/A:1020236927814
DO - 10.1023/A:1020236927814
M3 - Article
C2 - 10213268
AN - SCOPUS:0032896798
VL - 23
SP - 117
EP - 129
JO - Inflammation
JF - Inflammation
SN - 0360-3997
IS - 2
ER -