Aso H, Tamura K, Yoshie O, Nakamura T, Kikuchi S, Ishida N
Department of Pharmaceutical Sciences, Tohoku University Hospital, Miyagi, Japan.
Microbiol Immunol. 1992;36(10):1087-97. doi: 10.1111/j.1348-0421.1992.tb02112.x.
In vitro NK responses of cancer patients (N = 21) to rIFN-alpha A 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 micrograms/ml to 470 micrograms/ml), had their NK activities significantly augmented by rIFN-alpha A and rIL-2. On the other hand, NK cells from ten out of fifteen patients whose serum IAP concentrations were 650 micrograms/ml or more, were not activated by rIFN-alpha A. NK cells of these fifteen patients yet were capable of responding to rIL-2. NK cells from cancer patients, however, became responsive to rIFN-alpha A 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-alpha A by an indomethacin-sensitive mechanisms. It was further shown that PGE2 was not the mediator of this suppression.
对21例癌症患者的体外自然杀伤（NK）细胞对重组α-A干扰素（rIFN-αA）和重组白细胞介素-2（rIL-2）的反应进行了检测。同时测定了免疫抑制酸性蛋白（IAP）的血清浓度。血清IAP含量在正常范围内（270微克/毫升至470微克/毫升）的7例患者中，有5例患者的NK活性被rIFN-αA和rIL-2显著增强。另一方面，血清IAP浓度为650微克/毫升或更高的15例患者中，有10例患者的NK细胞未被rIFN-αA激活。然而，这15例患者的NK细胞仍能对rIL-2作出反应。不过，癌症患者的NK细胞通过去除黏附细胞或用消炎痛处理后，对rIFN-αA产生反应。因此，血清IAP水平高的癌症患者外周血单核细胞（PBMC）中的巨噬细胞似乎通过一种消炎痛敏感的机制选择性地抑制NK细胞对rIFN-αA的反应。进一步表明，前列腺素E2不是这种抑制作用的介质。
