We investigated the effect of a monoclonal antibody against CD2 molecules (OX34) in preventing the induction of experimental autoimmune myocarditis (EAM) induced by immunizing Lewis rats with cardiac myosin. Administration of OX34 before immunization, on Days -6, -4, -2 and 0, completely prevented EAM. On the other hand, treatment with OX34 just before the appearance of myocardial lesions, on Days 9, 11, 13 and 15, had only a partial effect in preventing the disease. Flow cytometric analysis of lymph node cells showed that CD3+ T cells were immediately depleted with the administration of OX34 but had largely recovered on Day 21. Lymph node cells in OX34-treated rats had no proliferative responses to cardiac myosin-rod, but the proliferation was restored when recombinant IL-2 was added. Ultimate production of the anti-myosin antibody was not inhibited by the treatment with OX34. These results suggest that the prevention of EAM by administering the anti-CD2 monoclonal antibody OX34 resulted from T cell depletion during the induction phase, and might in addition result from T cell anergy of Th1, but not Th2 cells.

译文

我们研究了针对CD2分子 (OX34) 的单克隆抗体在预防通过用心脏肌球蛋白免疫Lewis大鼠诱导的实验性自身免疫性心肌炎 (EAM) 中的作用。预防接种,在-6、-4、-2和0天给予OX34,完全预防了EAM。另一方面,在心肌病变出现之前,在第9、11、13和15天,用OX34治疗仅对预防该疾病有部分作用。淋巴结细胞的流式细胞术分析表明,CD3 T细胞在OX34的给药后立即耗尽,但在第21天已基本恢复。OX34-treated大鼠的淋巴结细胞对心肌肌球蛋白棒没有增殖反应,但添加重组IL-2后增殖得以恢复。用ox34处理不会抑制抗肌球蛋白抗体的最终产生。这些结果表明,通过施用anti-CD2单克隆抗体OX34来预防EAM是由于诱导期T细胞耗竭引起的,并且可能另外是由于Th1的T细胞无反应性,而不是Th2细胞。

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