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机构地区:[1]海军医学研究所同位素实验中心,上海200433 [2]第二军医大学放射医学研究室
出 处:《第二军医大学学报》1990年第4期325-327,共3页Academic Journal of Second Military Medical University
摘 要:紫色杆菌内毒素(LPS)处理供体小鼠能抑制移植物抗宿主反应(GVHR)。本文对其免疫学机理进行了初步探讨。结果表明,LPS能促进小鼠脾细胞的增殖,但降低其对Con A和LPS的反应性以及抑制MLR和NK细胞活性,利用混合培养方法发现,LPS对MLR和NK细胞活性的抑制作用不是由抑制细胞所介导,提示LPS预防GVHD是通过非抑制细胞途径抑制了T、NK细胞的功能而实现的。We had confirmed that treatment of donor mice with Ch. Violaceum endotoxin (lipopolysacchari-de,LPS)could inhibit GVHR. In this paper, its immunological mechanisms were explored. The results showed that the LPS could augment [3H] -TdR uptake by mouse spleen cells, but decrease their proliferative responses to LPS and Con A, and suppress unidirectional MLR and NK cell activity, with inhibitory rate of 64.5%, 66.1%, 51.7% and 59.3%, respectively, suggesting it had inhibitory effects on B, T lymphocytes and NK cells. In vitro experiments using mixtures of spleen cells from treated and normal mice showed there existed non-specific suppressor cell activity in LPS-and Con A-induced lymphocyte transformation but not in MLR and NK activity assays. That meant suppressor cells were not responsible for suppressive effects on T cells and NK cells which are thought to be main effector cells mediating GVHD.
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