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腺苷类似物对膜磷脂甲基化的改变不影响T淋巴细胞的激活。

Alteration of membrane phospholipid methylation by adenosine analogs does not affect T lymphocyte activation.

作者信息

Gormand F, Cordier G, Fonlupt P, Pacheco Y, Revillard J P

机构信息

Service de Pneumologie, Centre Hospitalier Lyon Sud, Pierre Bénite, France.

出版信息

Life Sci. 1990;47(20):1793-9. doi: 10.1016/0024-3205(90)90281-u.

Abstract

Membrane phospholipid methylation has been described during activation of various immune cells. Moreover recent data indicated modulation of immune cells functions by adenosine. As S-Adenosyl-methionine and S-Adenosyl-homocysteine are adenosine analogs and modulators of transmethylation reactions, the effects of SAH and SAM were investigated on membrane phospholipid methylation and lymphocyte activation. SAM (10(-5) M) was shown to induce the membrane phospholipid methylation as assessed by the 3H-methyl-incorporation in membrane extract. This effect was inhibited by SAH. In contrast SAM and SAH did not affect the phytohemagglutinin-induced proliferative response of peripheral blood mononuclear cells. SAH neither modified the early internalization of membrane CD3 antigens nor did it prevent the late expression of HLA-DR antigens on lymphocytes activated by phytohemagglutinin. These results indicate that in vitro alteration of phospholipid methylation does not affect subsequent steps of human T lymphocyte activation and proliferation.

摘要

在各种免疫细胞激活过程中,已发现存在膜磷脂甲基化现象。此外,最近的数据表明腺苷可调节免疫细胞功能。由于S-腺苷甲硫氨酸和S-腺苷高半胱氨酸是腺苷类似物以及转甲基化反应的调节剂,因此研究了SAH和SAM对膜磷脂甲基化及淋巴细胞激活的影响。通过测定膜提取物中3H-甲基掺入量评估发现,SAM(10(-5) M)可诱导膜磷脂甲基化。SAH可抑制这一效应。相比之下,SAM和SAH并不影响植物血凝素诱导的外周血单个核细胞增殖反应。SAH既不改变膜CD3抗原的早期内化,也不能阻止植物血凝素激活的淋巴细胞上HLA-DR抗原的后期表达。这些结果表明,体外磷脂甲基化的改变并不影响人T淋巴细胞激活和增殖的后续步骤。

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