In vitro NK responses of cancer patients (AT=21) to rIFN-aA and rIL-2 were examined. The serum concentration of IAP (immunosuppressive acidic protein) was determined in parallel. Five out of seven patients whose serum IAP contents were within the normal range (270 μg/ml to 470 μg/ml), had their NK activities significantly augmented by rIFN-αA and rIL-2. On the other hand, NK cells from ten out of fifteen patients whose serum IAP concentrations were 650 μg/ ml or more, were not activated by rIFN-αA. NK cells of these fifteen patients yet were capable of responding to rIL-2. NK cells from cancer patients, however, became responsive to rIFN-aA by either removal of adherent cells or treatment with indomethacin. Therefore, macrophages in PBMC of cancer patients with high serum IAP levels seem to selectively suppress NK response to rIFN-aA by an indomethacin-sensitive mechanisms. It was further shown that PGE2 was not the mediator of this suppression.
|Number of pages||13|
|Journal||MICROBIOLOGY and IMMUNOLOGY|
|Publication status||Published - 1992 Jan 1|
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