Prostaglandin E2 from macrophages of murine splenocyte cultures inhibits the generation of lymphokine-activated killer cell activity.
Prostaglandin E2 from macrophages of murine splenocyte cultures inhibits the generation of lymphokine-activated killer cell activity.
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来自小鼠脾细胞培养物巨噬细胞的前列腺素 E2 抑制淋巴因子激活的杀伤细胞活性的产生。
DOI:
10.1159/000217694
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发表时间:
1991
期刊:
影响因子:
--
通讯作者:
Chu,TM
中科院分区:
文献类型:
--
作者:
Ohnishi,H;Lin,TH;Nakajima,I;Chu,TM
The present work investigated the association between prostaglandin E2(PGE2) from macrophages and its inhibition of murine lymphokine-activated killer (LAK) cell generation. The coculture of indomethacin with interleukin-2 (IL-2) augmented LAK cell activity in an indomethacin dose-response manner, and diminished PGE2content in the corresponding culture supernatant in a reverse dose-response manner. The correlation between the increase in LAK cell activity and the decrease in PGE2content was highly significant. Identical results were obtained with diclofenac. A profound inhibition of LAK cell activity by exogenous PGE2in a dose-response manner was detected. Polyclonal anti-PGE2antiserum augmented in a dose-dependent manner the LAK cell activity, by neutralizing PGE2in the medium. A reduction of PGE2content in the culture supernatant was also detected when the macrophage subpopulations were cultured and was indomethacin dose-dependent. In comparison with that of normal mouse splenocytes, the incubation of whole splenocytes of tumor-bearing mice, which contained a greater subpopulation of macrophages (24% vs. 12 %), produced a greater PGE2content and a correspondingly depressed LAK cell activity. Additionally, PGE2reduced protein kinase C (PKC) activity along with LAK cell activity generated from macrophage-depleted T cells and natural-killer-like cells. These results overall indicate that PGE2from macrophages in murine splenocyte cultures inhibits the LAK cell generation, and PKC may be involved in the inhibition mechanism.