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用杜氏利什曼原虫前鞭毛体接种人单核细胞产生的一种可溶性因子可抑制IFN-γ依赖的单核细胞活化。

A soluble factor produced by inoculation of human monocytes with Leishmania donovani promastigotes suppresses IFN-gamma-dependent monocyte activation.

作者信息

Engelhorn S, Bruckner A, Remold H G

机构信息

Department of Rheumatology and Immunology, Brigham and Women's Hospital, Boston 02115.

出版信息

J Immunol. 1990 Oct 15;145(8):2662-8.

PMID:2120335
Abstract

Whereas human cultured monocytes preactivated with IFN-gamma increase their antileishmanial capacity, monocytes inoculated with Leishmania donovani before IFN-gamma treatment fail to respond with an increase of antileishmanial capacity. Cell surface expression of class II MHC products also fails to be increased by IFN-gamma in the infected monocytes, although the accumulation of HLA-DR alpha-chain mRNA is increased to the same extent in infected and noninfected activated monocytes. This inhibition of monocyte activation is caused in a dose-dependent manner by a soluble substance elaborated into the cell supernatant after inoculation of monocytes with L. donovani and is referred to as activation suppressing factor (ASF). ASF activity can be abrogated by dialysis and by treatment with a proteinase, indicating that ASF is a small peptide.

摘要

虽然用γ干扰素预激活的人培养单核细胞会增强其抗利什曼原虫能力,但在γ干扰素处理前接种杜氏利什曼原虫的单核细胞,其抗利什曼原虫能力并不会增强。在受感染的单核细胞中,γ干扰素也无法增加Ⅱ类MHC产物的细胞表面表达,尽管在受感染和未受感染的活化单核细胞中,HLA-DRα链mRNA的积累增加程度相同。这种单核细胞活化的抑制是由接种杜氏利什曼原虫后分泌到细胞上清液中的一种可溶性物质以剂量依赖方式引起的,该物质被称为活化抑制因子(ASF)。ASF活性可通过透析和蛋白酶处理消除,这表明ASF是一种小肽。

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A soluble factor produced by inoculation of human monocytes with Leishmania donovani promastigotes suppresses IFN-gamma-dependent monocyte activation.用杜氏利什曼原虫前鞭毛体接种人单核细胞产生的一种可溶性因子可抑制IFN-γ依赖的单核细胞活化。
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Phagocytosis of the malarial pigment, hemozoin, impairs expression of major histocompatibility complex class II antigen, CD54, and CD11c in human monocytes.疟色素(疟原虫血色素)的吞噬作用会损害人类单核细胞中主要组织相容性复合体II类抗原、CD54和CD11c的表达。
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Leishmaniases of the New World: current concepts and implications for future research.
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Clin Microbiol Rev. 1993 Jul;6(3):230-50. doi: 10.1128/CMR.6.3.230.