Kokudo S, Chu T M
Department of Diagnostic Immunology Research and Biochemistry, Roswell Park Cancer Institute, New York State Department of Health, Buffalo 14263.
Tumour Biol. 1993;14(3):144-54. doi: 10.1159/000217830.
To elucidate the inhibitory effect of prostaglandin E2 (PGE2) on the generation of recombinant interleukin-2 (IL-2)-induced lymphokine-activated killer (LAK) activity, we have examined the association between cellular 3',5'-cyclic adenosine monophosphate (cAMP) and cytolytic activity of 3-day IL-2-cultured murine LAK cells, i.e. at late phase of IL-2 induction, in the presence and absence of PGE2. The results indicate that, at the late phase of IL-2 induction, LAK cells retain their responsiveness to PGE2 inhibition, and the inhibition can be partially suppressed by additional IL-2 in proportion to the decrease in the ratios of stimulated to basal cellular cAMP levels.
为了阐明前列腺素E2(PGE2)对重组白细胞介素-2(IL-2)诱导的淋巴因子激活的杀伤细胞(LAK)活性产生的抑制作用,我们研究了细胞3',5'-环磷酸腺苷(cAMP)与经3天IL-2培养的小鼠LAK细胞(即在IL-2诱导后期)在有或无PGE2存在情况下的细胞溶解活性之间的关联。结果表明,在IL-2诱导后期,LAK细胞仍保持对PGE2抑制的反应性,并且该抑制作用可被额外添加的IL-2部分抑制,抑制程度与受刺激细胞cAMP水平与基础细胞cAMP水平之比的降低成比例。