Effect of morphine on cell-mediated immune responses of human lymphocytes against allogeneic malignant cells.
Effect of morphine on cell-mediated immune responses of human lymphocytes against allogeneic malignant cells.
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吗啡对人淋巴细胞针对同种异体恶性细胞的细胞介导的免疫反应的影响。
DOI：
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发表时间：
2005
期刊：
影响因子：
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通讯作者：
G. Lanzilli
中科院分区：
文献类型：
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作者：
M. Fuggetta;P. di Francesco;R. Falchetti;A. Cottarelli;L. Rossi;M. Tricarico;G. Lanzilli
阿片类药物，包括吗啡，主要用于肿瘤生长和进展不同阶段的癌症患者的疼痛控制。因此，这些药物对宿主免疫的可能影响似乎是相当大的兴趣。我们在体外研究了吗啡对HTLV-Ⅰ诱导的T细胞白血病细胞（MT-2细胞系）产生人细胞毒性T淋巴细胞（CTL）的影响。结果显示，药物在分级浓度（从3 μ g/ml到32 μ g/ml）下，包括在治疗患者中可检测到的那些，增强CTL活性，而自然杀伤细胞活性不受影响。当在淋巴细胞/MT-2共培养开始时存在吗啡时，增强效果特别明显。相反，当在共培养的最后一天加入时，药物是无效的，因此表明吗啡在CTL的生成阶段起作用，但不作用于成熟CTL。流式细胞术分析细胞内细胞因子的表达表明，吗啡增加了共培养试验中产生干扰素γ的CD 8 + T细胞的百分比。总的来说，这些结果表明，在我们的实验模型中，吗啡通过直接影响T依赖性细胞介导的免疫的诱导期来增强CTL应答。
Opioid drugs, including morphine, are largely used as pain control in cancer patients at different stages of neoplastic growth and progression. Therefore, the possible influence of these drugs on host immunity appears to be of considerable interest. We have examined in vitro the effect of morphine on the generation of human cytotoxic T lymphocytes (CTL) against HTLV-I induced T-cell leukemia cells (MT-2 line). The results show that the drug, at graded concentrations (from 3 pg/ml to 32 microg/ml), that include those detectable in treated patients, enhances CTL activity whereas natural killer cell activity was unaffected. The enhancing effect is particularly evident when morphine was present at the onset of lymphocyte/MT-2 co-culture. On the contrary, the drug was ineffective when added on the last day of co-culture, thus indicating that morphine operates during the generation phase of CTL, but not on mature CTL. Flow cytometric analysis of intracellular cytokine expression showed that morphine increases the percentage of interferon gamma-producing CD8+ T cells in co-culture assay. Collectively, these results suggest that in our experimental model morphine enhances CTL responses by directly affecting the induction phase of T-dependent cell-mediated immunity.