血管紧张素II对人单核细胞反应性的抑制与OKT8+淋巴细胞胸苷结合增强有关。

M. Simon, D. Engel, J. Weinstock
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引用次数: 10

摘要

最近的证据表明,血管紧张素II可能参与炎症的调节。我们以前报道过血管紧张素II抑制人外周血单核细胞的反应性,并直接作用于淋巴细胞。这些观察结果再次得到证实。此外,纯化的OKT8+而非OKT4+ T细胞悬液经植物血凝素刺激后,与血管紧张素II同时培养48小时后,胸腺嘧啶掺入增加。这些发现表明血管紧张素II可能通过刺激OKT8+亚群中的抑制性淋巴细胞来抑制单核细胞胸苷的摄取。
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Angiotensin II suppression of human mononuclear cell reactivity is associated with enhanced OKT8+ lymphocyte thymidine incorporation.
Recent evidence suggests that angiotensin II may participate in the regulation of inflammation. We previously reported that angiotensin II inhibits human peripheral blood mononuclear cell reactivity and acts directly on lymphocytes. These observations are again confirmed. In addition, purified OKT8+ but not OKT4+ T cell suspensions stimulated with phytohemagglutinin revealed increased thymidine incorporation when simultaneously cultured for 48 hours with angiotensin II. These findings suggest that angiotensin II may inhibit mononuclear cell thymidine uptake through stimulation of suppressor lymphocytes contained within the OKT8+ subpopulation.
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