TY - JOUR
T1 - Impaired Nk Response of Cancer Patients To Ifn-« But Not To Il-2
T2 - Correlation With Serum Immuno-suppressive Acidic Protein (iap) And Role of Suppressor Macrophage
AU - Aso, Hisashi
AU - Tamura, Keiji
AU - Nakamura, Takehiko
AU - Yoshie, Osamu
PY - 1992/1/1
Y1 - 1992/1/1
N2 - 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.
AB - 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.
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M3 - Article
AN - SCOPUS:85010104447
SN - 0385-5600
VL - 36
SP - 947
EP - 959
JO - Microbiology and Immunology
JF - Microbiology and Immunology
IS - 10
ER -