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恰加斯利什曼原虫感染会改变人单核细胞和巨噬细胞上细胞黏附分子和共刺激分子的表达。

Leishmania (Leishmania) chagasi infection alters the expression of cell adhesion and costimulatory molecules on human monocyte and macrophage.

作者信息

De Almeida M C, Cardoso S A, Barral-Netto M

机构信息

Faculdade de Medicina, Universidade Federal da Bahia Gonçalo Moniz, Fiocruz, Salvador, BA, Brazil.

出版信息

Int J Parasitol. 2003 Feb;33(2):153-62. doi: 10.1016/s0020-7519(02)00266-7.

DOI:10.1016/s0020-7519(02)00266-7
PMID:12633653
Abstract

The initial steps of Leishmania infection in humans are largely unknown. There is limited information on the Leishmania infected human monocytes, the first cells that the parasite lives in, particularly related to costimulatory molecules. We show here that Leishmania (L.) chagasi infection avoids inducing proinflammatory molecules and has striking down modulating effects on human monocytes or macrophages. It does not induce CD54, interleukin (IL)-12 or tumour necrosis factor-alpha, potent proinflammatory cytokines and down modulates CD11b expression in monocytes. Lipopolysaccharide stimulated IL-12 (p40) levels, CD54 and HLA-DR expression are diminished in infected monocytes as well as interferon-gamma stimulated HLA-DR and HLA-ABC expression in infected macrophages. There is a negative correlation between CD54 and CD86 expression in both monocytes and macrophages. The depressed expression of class I and II molecules, absence of key proinflammatory cytokines and impaired expression of costimulatory molecules induced by L. chagasi could leave the immune system, at least in its initial phases in anergy or ignorance.

摘要

利什曼原虫在人体内的初始感染步骤在很大程度上尚不清楚。关于被利什曼原虫感染的人类单核细胞(寄生虫最初寄生的细胞)的信息有限,尤其是与共刺激分子相关的信息。我们在此表明,恰加斯利什曼原虫感染可避免诱导促炎分子,并对人类单核细胞或巨噬细胞具有显著的下调作用。它不会诱导CD54、白细胞介素(IL)-12或肿瘤坏死因子-α(强效促炎细胞因子),并下调单核细胞中CD11b的表达。在受感染的单核细胞中,脂多糖刺激的IL-12(p40)水平、CD54和HLA-DR表达降低,在受感染的巨噬细胞中,干扰素-γ刺激的HLA-DR和HLA-ABC表达也降低。在单核细胞和巨噬细胞中,CD54和CD86表达之间均呈负相关。恰加斯利什曼原虫诱导的I类和II类分子表达降低、关键促炎细胞因子缺失以及共刺激分子表达受损,可能会使免疫系统至少在其初始阶段处于无反应或忽视状态。

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