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内毒素与淋巴因子协同激活小鼠巨噬细胞系J774抵抗克氏锥虫感染的作用

Activation by synergism between endotoxin and lymphokines of the mouse macrophage cell line J774 against infection by Trypanosoma cruzi.

作者信息

Alcina A, Fresno M

出版信息

Parasite Immunol. 1987 Mar;9(2):175-86. doi: 10.1111/j.1365-3024.1987.tb00498.x.

DOI:10.1111/j.1365-3024.1987.tb00498.x
PMID:3106922
Abstract

The mouse macrophage cell line J774 was easily infected by T. cruzi epimastigotes which were transformed to amastigotes that multiplied inside the cells. Spleen-T-cells from T. cruzi immune mice stimulated with Concanavalin A or T. cruzi, but not with unrelated antigens, released lymphokines into the supernatants that when added to J774 cells were unable to induce complete trypanocidal activity, although they were able to delay the rate of infection by protecting the cells from being infected. Addition of bacterial lipopolysaccharide (LPS), although inactive by itself, acted synergistically with the supernatants in inducing complete trypanocidal activity without affecting the susceptibility of J774 cells to infection. Gamma-interferon (gamma-IFN) activity was detected in the supernatants, however, but was not solely responsible for the trypanocidal inducing activities, since: there was no correlation between the levels of gamma-IFN and macrophage activation; gamma-IFN alone was less effective than the supernatants alone; and two active fractions of 100,000-150,000 mol. wt and 30,000 mol. wt were separated by gel filtration chromatography of the lymphokine preparations. The latter, which showed the characteristics of gamma-IFN with respect to size, pH 2 sensitivity and antiviral activity, had some trypanocidal activity alone. However, the 100,000-150,000 mol. wt fraction was active only in the presence of LPS. Finally, this trypanocidal inducing activity of the supernatants was not due to the induction of synthesis of gamma-IFN by the J774 cells.

摘要

小鼠巨噬细胞系J774很容易被克氏锥虫前鞭毛体感染,这些前鞭毛体转化为无鞭毛体并在细胞内增殖。用刀豆球蛋白A或克氏锥虫刺激,但不用无关抗原刺激的来自克氏锥虫免疫小鼠的脾T细胞,会将淋巴因子释放到上清液中。当将这些上清液添加到J774细胞中时,虽然它们能够通过保护细胞不被感染来延迟感染率,但却无法诱导出完全的杀锥虫活性。添加细菌脂多糖(LPS),尽管其本身无活性,但与上清液协同作用可诱导出完全的杀锥虫活性,而不影响J774细胞对感染的易感性。然而,在上清液中检测到了γ-干扰素(γ-IFN)活性,但它并非杀锥虫诱导活性的唯一原因,因为:γ-IFN水平与巨噬细胞活化之间没有相关性;单独的γ-IFN比单独的上清液效果要差;通过对淋巴因子制剂进行凝胶过滤层析,分离出了分子量为100,000 - 150,000和30,000的两个活性组分。后者在大小、对pH 2的敏感性和抗病毒活性方面表现出γ-IFN的特征,单独具有一定的杀锥虫活性。然而,分子量为100,000 - 150,000的组分仅在LPS存在时才有活性。最后,上清液的这种杀锥虫诱导活性并非由于J774细胞诱导合成γ-IFN所致。

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Activation by synergism between endotoxin and lymphokines of the mouse macrophage cell line J774 against infection by Trypanosoma cruzi.内毒素与淋巴因子协同激活小鼠巨噬细胞系J774抵抗克氏锥虫感染的作用
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PLoS Pathog. 2012;8(7):e1002799. doi: 10.1371/journal.ppat.1002799. Epub 2012 Jul 12.
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Dominant T- and B-cell epitopes in an autoantigen linked to Chagas' disease.与恰加斯病相关的自身抗原中的显性T细胞和B细胞表位。
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Interferon-gamma-activated immature macrophages exhibit a high Trypanosoma cruzi infection rate associated with a low production of both nitric oxide and tumor necrosis factor-alpha.
γ-干扰素激活的未成熟巨噬细胞表现出高克氏锥虫感染率,同时一氧化氮和肿瘤坏死因子-α的产生量较低。
Parasitol Res. 1994;80(7):554-8. doi: 10.1007/BF00933002.
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Activity of P536, a UDP-glucose analog, against Trypanosoma cruzi.UDP-葡萄糖类似物P536对克氏锥虫的活性。
Antimicrob Agents Chemother. 1988 Sep;32(9):1412-5. doi: 10.1128/AAC.32.9.1412.
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Characterization of a glycosyl-phosphatidylinositol-anchored membrane protein from Trypanosoma cruzi.克氏锥虫糖基磷脂酰肌醇锚定膜蛋白的特性分析
Infect Immun. 1991 Apr;59(4):1409-16. doi: 10.1128/iai.59.4.1409-1416.1991.
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Trypanosoma cruzi but not Trypanosoma brucei fails to induce a chemiluminescent signal in a macrophage hybridoma cell line.克氏锥虫而非布氏锥虫无法在巨噬细胞杂交瘤细胞系中诱导化学发光信号。
Infect Immun. 1991 Sep;59(9):3303-8. doi: 10.1128/iai.59.9.3303-3308.1991.