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首页> 外文期刊>International journal of immunopharmacology >Paclitaxel causes mouse splenic lymphocytes to a state hyporesponsive to lipopolysaccharide stimulation.
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Paclitaxel causes mouse splenic lymphocytes to a state hyporesponsive to lipopolysaccharide stimulation.

机译：紫杉醇使小鼠脾淋巴细胞的状态对脂多糖刺激反应低下。

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Multiple immune system actions have been ascribed to paclitaxel (taxol), a novel anticancer drug, including the capacity to induce macrophage antitumor cytotoxic molecule production. In the present studies, we demonstrated that paclitaxel produced a selective inhibition of lipopolysaccharide (LPS)-induced B cell proliferation. Similarly, in vitro polyclonal antibody-forming cell responses also were found to be inhibited by paclitaxel. Conversely, paclitaxel exhibited no inhibitory effects on concanavalin A (Con A)-induced T cell proliferation. To study the pathway leading to paclitaxel-induced immunosuppression, we analyzed Raf-1/ERK and JNK/p38 MAPK pathways, both of which have been reported to be involved in LPS signaling. Our results indicate that taxol treatment inhibits Raf-1 kinase activation while having no effect on ERK activation suggesting that ERK activation is distinct from upstream Raf-1 kinase in taxol-induced immunomodulation. Furthermore, paclitaxel pretreatment caused down-regulation of stress-activated MAPKs, JNK and p38 MAPK in lipopolysaccharide (LPS)-stimulated mouse splenic lymphocytes, demonstrating that spleen cells are induced to a state hyporesponsive to LPS stimulation by pre-exposing them to paclitaxel. Taken together, these results suggest that down-regulation of JNK/p38 MAP kinase may contribute to paclitaxel-induced immunosuppression in mouse splenic lymphocytes.
机译：紫杉醇（紫杉醇）是一种新型抗癌药物，具有多种免疫系统作用，包括诱导巨噬细胞抗肿瘤细胞毒性分子产生的能力。在本研究中，我们证明了紫杉醇产生选择性抑制脂多糖（LPS）诱导的B细胞增殖。同样，紫杉醇也能抑制体外形成多克隆抗体的细胞反应。相反，紫杉醇对伴刀豆球蛋白A（Con A）诱导的T细胞增殖没有抑制作用。为了研究导致紫杉醇诱导的免疫抑制的途径，我们分析了Raf-1 / ERK和JNK / p38 MAPK途径，据报道这两种途径均参与LPS信号传导。我们的结果表明紫杉醇治疗抑制Raf-1激酶激活，而对ERK激活没有影响，这表明ERK激活在紫杉醇诱导的免疫调节中不同于上游Raf-1激酶。此外，紫杉醇预处理导致脂多糖（LPS）刺激的小鼠脾淋巴细胞中应激激活的MAPK，JNK和p38 MAPK的下调，表明脾细胞通过将它们预先暴露于紫杉醇而被诱导为对LPS刺激反应低的状态。综上所述，这些结果表明JNK / p38 MAP激酶的下调可能有助于紫杉醇诱导的小鼠脾淋巴细胞的免疫抑制。

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