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Abstract

The in vitro effect of C-AGP (pure alpha1-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 NK cell activity by rIFNalphaA and rIFNgamma, 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 rIFNalphaA. However, after the treatment of PBMC with C-AGP for 5 or 6 days, NK cells failed to respond to rIFNalphaA, in spite of washing to remove C-AGP from the cultures. Monocytes were necessary for the suppressive effect of C-AGP on rIFNalphaA activation of NK cells. Indomethacin restored the ability of NK cells to respond to rIFNalphaA 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.

The Acute Phase Protein α1-Acid Glycoprotein: A Model for Altered Glycosylation During Diseases

“…C-AGP had no effect on basal activity of NK, but inhibited the increase of NK cytotoxicity induced by recombinant IFN and IFN . It was also found that this suppressive activity of C-AGP on NK cells was mediated by monocytes, and could be restored after incubation with the non-steroidal anti-inflammatory drug Indomethacin [150].…”