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自然杀伤细胞参与小鼠对利什曼原虫主要感染的早期防御。

Natural killer cells participate in the early defense against Leishmania major infection in mice.

作者信息

Laskay T, Röllinghoff M, Solbach W

机构信息

Institute for Clinical Microbiology, University of Erlangen-Nürnberg, FRG.

出版信息

Eur J Immunol. 1993 Sep;23(9):2237-41. doi: 10.1002/eji.1830230928.

Abstract

In this study the role of natural killer (NK) cells in the course of experimental Leishmania major infection was investigated. NK cells in genetically resistant C57BL/6 mice were depleted by in vivo administration of anti-asialo-GM1 or anti-NK1.1 antibodies. A marked exacerbation of the infection was found in the NK-depleted mice within the first two weeks of infection. Both the local tissue swelling and the number of parasites in the lesions were significantly higher than in normal animals. Lymph node cells taken from infected NK-depleted mice released less interferon-gamma (IFN-gamma) when cultured in vitro. As an alternate approach we have used poly I:C treatment in order to activate NK cell activity in vivo in BALB/c mice, which are genetically susceptible to L. major infection. Poly I:C treatment led to milder symptoms and to a significantly lower parasite burden in the early course of infection. Lymph node cells from infected and poly I:C-treated BALB/c mice released higher amount of IFN-gamma in vitro than cells from control mice. These data show that NK cells are active participants in the non-specific phase of anti-leishmanial activity in the control of parasite multiplication early in the course of L. major infection in mice.

摘要

在本研究中,对自然杀伤(NK)细胞在实验性硕大利什曼原虫感染过程中的作用进行了研究。通过体内给予抗去唾液酸GM1或抗NK1.1抗体,使基因抗性C57BL/6小鼠体内的NK细胞耗竭。在感染的前两周内,NK细胞耗竭的小鼠出现了感染的明显加重。局部组织肿胀和病变中的寄生虫数量均显著高于正常动物。从感染的NK细胞耗竭小鼠获取的淋巴结细胞在体外培养时释放的γ干扰素(IFN-γ)较少。作为另一种方法,我们使用聚肌胞苷酸(poly I:C)处理,以在体内激活对硕大利什曼原虫感染具有遗传易感性的BALB/c小鼠的NK细胞活性。Poly I:C处理导致在感染早期症状较轻且寄生虫负荷显著降低。与对照小鼠的细胞相比,来自感染且经poly I:C处理的BALB/c小鼠的淋巴结细胞在体外释放的IFN-γ量更高。这些数据表明,在小鼠硕大利什曼原虫感染过程早期,NK细胞是控制寄生虫增殖的抗利什曼原虫非特异性活性阶段的积极参与者。

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