Ethanol impairs major histocompatibility complex (MHC) class II molecule-mediated but not MHC class I molecule-mediated T cell response in alcohol-consuming mice
Ethanol impairs major histocompatibility complex (MHC) class II molecule-mediated but not MHC class I molecule-mediated T cell response in alcohol-consuming mice
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DOI：
10.3109/08923979909016395
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发表时间：
1999-01-01
影响因子：
3.3
通讯作者：
Norman, DC
中科院分区：
文献类型：
--
作者：
Chang, MP;Norman, DC
本研究的目的是确定酒精是否会影响小鼠同种异体抗原诱导的T细胞增殖和细胞溶解活性，以及这种改变的免疫反应是否部分是由于IL-2活性的缺陷造成的。研究了C57BL/6小鼠的脾脏细胞产生同种异体特异性混合淋巴细胞反应（MLR）和细胞毒性T淋巴细胞（CTL）的能力，并与正常饮食和等热量麦芽糖饮食的小鼠进行了比较。通过使C57BL/6小鼠脾细胞对BALB/c小鼠脾细胞致敏产生同种异体MLR和CTL，并通过CTL杀伤cr -51标记的P815肥大细胞瘤靶细胞的能力来确定同种异体特异性CTL活性。我们的研究结果显示，酒精摄入小鼠应答细胞的同种异体特异性MLR显著降低（降低40%，p0.05）。最后，我们还证明了乙醇不会损害混合淋巴细胞培养中异体抗原诱导的IL-2产生（P < 0.01）。
The goal of this study was to determine whether alcohol affects alloantigen-induced proliferative and cytolytic activity of T cells in mice, and whether the altered immune response was in part due to a defect of IL-2 activity. The ability of spleen cells from individual alcohol-consuming C57BL/6 mice to generate allo-specific mixed lymphocyte response (MLR) and cytotoxic T lymphocyte (CTL) was compared to that of mice fed on an isocaloric maltose diet and regular diet. Allospecific MLR and CTL were generated by sensitizing spleen cells of C57BL/6 mice against spleen cells from BALB/c mice, and the allo-specific CTL activity was determined by the ability of the CTL to kill Cr-51-labeled P815 mastocytoma target cells. Our results showed that the allo-specific MLR of the responder cells from alcohol-consuming mice was significantly reduced (40% reduction, p0.05). Finally, we also demonstrated that ethanol did not impair the alloantigen-induced IL-2 production in the mixed lymphocyte cultures (P>0.1).