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本文引用的文献

1
Infection of C57BL/10ScCr and C57BL/10ScNCr mice with Leishmania major reveals a role for Toll-like receptor 4 in the control of parasite replication.用硕大利什曼原虫感染C57BL/10ScCr和C57BL/10ScNCr小鼠，揭示了Toll样受体4在控制寄生虫复制中的作用。
J Leukoc Biol. 2004 Jul;76(1):48-57. doi: 10.1189/jlb.1003484. Epub 2004 Mar 23.
2
Toll-like receptor 4 contributes to efficient control of infection with the protozoan parasite Leishmania major.Toll样受体4有助于有效控制原生动物寄生虫硕大利什曼原虫的感染。
Infect Immun. 2004 Apr;72(4):1920-8. doi: 10.1128/IAI.72.4.1920-1928.2004.
3
Myd88-dependent in vivo maturation of splenic dendritic cells induced by Leishmania donovani and other Leishmania species.杜氏利什曼原虫及其他利什曼原虫物种诱导的脾树突状细胞依赖髓样分化因子88的体内成熟
Infect Immun. 2004 Feb;72(2):824-32. doi: 10.1128/IAI.72.2.824-832.2004.
4
High levels of susceptibility and T helper 2 response in MyD88-deficient mice infected with Leishmania major are interleukin-4 dependent.感染杜氏利什曼原虫的MyD88缺陷小鼠中高水平的易感性和辅助性T细胞2反应依赖于白细胞介素-4。
Infect Immun. 2003 Dec;71(12):7215-8. doi: 10.1128/IAI.71.12.7215-7218.2003.
5
Differential production of macrophage inflammatory protein 1gamma (MIP-1gamma), lymphotactin, and MIP-2 by CD4(+) Th subsets polarized in vitro and in vivo.体外和体内极化的CD4(+) Th亚群对巨噬细胞炎性蛋白1γ（MIP-1γ）、淋巴细胞趋化因子和MIP-2的差异产生。
Infect Immun. 2003 Nov;71(11):6178-83. doi: 10.1128/IAI.71.11.6178-6183.2003.
6
MyD88 is essential for clearance of Leishmania major: possible role for lipophosphoglycan and Toll-like receptor 2 signaling.髓样分化因子88（MyD88）对于清除硕大利什曼原虫至关重要：脂磷壁酸聚糖和Toll样受体2信号传导的潜在作用
Eur J Immunol. 2003 Oct;33(10):2822-31. doi: 10.1002/eji.200324128.
7
Leishmania lipophosphoglycan (LPG) activates NK cells through toll-like receptor-2.利什曼原虫脂磷壁酸聚糖（LPG）通过Toll样受体2激活自然杀伤细胞。
Mol Biochem Parasitol. 2003 Aug 31;130(2):65-74. doi: 10.1016/s0166-6851(03)00160-9.
8
Impaired expression of inflammatory cytokines and chemokines at early stages of infection with Leishmania amazonensis.亚马逊利什曼原虫感染早期炎症细胞因子和趋化因子表达受损。
Infect Immun. 2003 Aug;71(8):4278-88. doi: 10.1128/IAI.71.8.4278-4288.2003.
9
Toll-like receptors stimulate human neutrophil function.Toll样受体刺激人类中性粒细胞功能。
Blood. 2003 Oct 1;102(7):2660-9. doi: 10.1182/blood-2003-04-1078. Epub 2003 Jun 26.
10
The Toll-like receptor 5 stimulus bacterial flagellin induces maturation and chemokine production in human dendritic cells.Toll样受体5刺激物细菌鞭毛蛋白可诱导人树突状细胞成熟并产生趋化因子。
J Immunol. 2003 May 15;170(10):5165-75. doi: 10.4049/jimmunol.170.10.5165.

感染硕大利什曼原虫的Toll样受体功能正常和缺陷小鼠中趋化因子基因的表达

Chemokine gene expression in toll-like receptor-competent and -deficient mice infected with Leishmania major.

作者信息

Antoniazi Simone, Price Helen P, Kropf Pascale, Freudenberg Marina A, Galanos Chris, Smith Deborah F, Müller Ingrid

机构信息

Imperial College London, Faculty of Medicine, Department of Immunology, Norfolk Place, London W2 1PG, United Kingdom.

出版信息

Infect Immun. 2004 Sep;72(9):5168-74. doi: 10.1128/IAI.72.9.5168-5174.2004.

DOI:10.1128/IAI.72.9.5168-5174.2004
PMID:15322011
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC517484/
Abstract

We studied the expression of a subset of chemokines, including RANTES/CCL5, MIP-1alpha/CCL3, IP-10/CXCL10, and MCP-1/CCL2, in Toll-like receptor (TLR)-competent and -deficient mice after infection with Leishmania major. Chemokine expression at the site of infection (the footpad), in the draining lymph nodes and in the spleens of infected animals was determined by using two different methods of analysis. The results indicate that L. major infection causes overall upregulation of RANTES/CCL5, MIP-1alpha/CCL3, IP-10/CXCL10, and MCP-1/CCL2 in the footpads and lymph nodes, while expression of these chemokines is constitutive in the spleens of TLR4-competent mice (C57BL/10ScSn) and TLR4-deficient mice (C57BL10/ScN). Different patterns of expression were detected depending on the time postinfection, but there was little variation in the expression of these four chemokines in the presence or absence of TLR4.

摘要

我们研究了在感染硕大利什曼原虫后，趋化因子的一个子集（包括RANTES/CCL5、MIP-1α/CCL3、IP-10/CXCL10和MCP-1/CCL2）在Toll样受体（TLR）功能正常和缺陷小鼠中的表达情况。通过两种不同的分析方法确定了感染动物的感染部位（足垫）、引流淋巴结和脾脏中的趋化因子表达。结果表明，硕大利什曼原虫感染导致足垫和淋巴结中RANTES/CCL5、MIP-1α/CCL3、IP-10/CXCL10和MCP-1/CCL2总体上调，而这些趋化因子在TLR4功能正常的小鼠（C57BL/10ScSn）和TLR4缺陷的小鼠（C57BL10/ScN）脾脏中是组成性表达的。根据感染后的时间检测到不同的表达模式，但在有或没有TLR4的情况下，这四种趋化因子的表达几乎没有差异。