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Suppressor macrophages in African trypanosomiasis inhibit T cell proliferative responses by nitric oxide and prostaglandins.非洲锥虫病中的抑制性巨噬细胞通过一氧化氮和前列腺素抑制T细胞增殖反应。
J Immunol. 1993 Nov 15;151(10):5492-503.
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Cultivation in a semi-defined medium of animal infective forms of Trypanosoma brucei, T. equiperdum, T. evansi, T. rhodesiense and T. gambiense.在半限定培养基中培养布氏锥虫、马媾疫锥虫、伊氏锥虫、罗德西亚锥虫和冈比亚锥虫的动物感染性形态。
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Dual role of macrophages in the suppression of interleukin 2 production and interleukin 2 receptor expression in trypanosome-infected mice.巨噬细胞在锥虫感染小鼠中抑制白细胞介素2产生及白细胞介素2受体表达的双重作用
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Macrophages as mediators of immunosuppression in murine African trypanosomiasis.巨噬细胞作为小鼠非洲锥虫病免疫抑制的介质
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Regional haemodynamic changes during oral ingestion of NG-monomethyl-L-arginine or NG-nitro-L-arginine methyl ester in conscious Brattleboro rats.清醒的遗传性高血压大鼠口服NG-单甲基-L-精氨酸或NG-硝基-L-精氨酸甲酯期间的局部血流动力学变化
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Biosynthesis and metabolism of endothelium-derived nitric oxide.
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Suppressive macrophages occurring in murine Trypanosoma brucei infection inhibit T-cell responses in vivo and in vitro.
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Macrophage cytostatic effect on Trypanosoma musculi involves an L-arginine-dependent mechanism.巨噬细胞对鼠锥虫的细胞抑制作用涉及一种依赖L-精氨酸的机制。
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一氧化氮合成的抑制导致小鼠布氏锥虫感染中寄生虫血症降低。

Inhibition of nitric oxide synthesis leads to reduced parasitemia in murine Trypanosoma brucei infection.

作者信息

Sternberg J, Mabbott N, Sutherland I, Liew F Y

机构信息

Department of Zoology, University of Aberdeen, Scotland.

出版信息

Infect Immun. 1994 May;62(5):2135-7. doi: 10.1128/iai.62.5.2135-2137.1994.

DOI:10.1128/iai.62.5.2135-2137.1994
PMID:8168985
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC186483/
Abstract

In murine Trypanosoma brucei infection, macrophage activation and nitric oxide (NO) production lead to suppressed splenic T-cell responses (J. Sternberg and F. McGuigan, Eur. J. Immunol. 22:2741-2744, 1992). In this study, evidence is presented that NO has no detectable trypanocidal activity under simulated in vivo conditions and that inhibition of NO production in vivo results in reduced parasitemia.

摘要

在小鼠布氏锥虫感染中,巨噬细胞激活和一氧化氮(NO)生成会导致脾脏T细胞反应受到抑制(J. 斯特恩伯格和F. 麦奎根,《欧洲免疫学杂志》22:2741 - 2744,1992年)。在本研究中,有证据表明,在模拟的体内条件下,NO没有可检测到的杀锥虫活性,并且体内抑制NO生成会导致寄生虫血症降低。