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本文引用的文献

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Distinct NKT cell subsets are induced by different Chlamydia species leading to differential adaptive immunity and host resistance to the infections.不同的衣原体物种可诱导不同的自然杀伤T细胞亚群,从而导致适应性免疫的差异以及宿主对感染的抵抗力不同。
J Immunol. 2007 Jan 15;178(2):1048-58. doi: 10.4049/jimmunol.178.2.1048.
2
Role of CCL5 (RANTES) in viral lung disease.CCL5(调节激活正常T细胞表达和分泌因子)在病毒性肺部疾病中的作用。
J Virol. 2006 Aug;80(16):8151-7. doi: 10.1128/JVI.00496-06.
3
Prior exposure to infection with Chlamydia pneumoniae can influence the T-cell-mediated response to Chlamydia trachomatis.先前感染肺炎衣原体可影响T细胞介导的对沙眼衣原体的反应。
FEMS Immunol Med Microbiol. 2006 Jul;47(2):190-8. doi: 10.1111/j.1574-695X.2006.00080.x.
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Immunology of Chlamydia infection: implications for a Chlamydia trachomatis vaccine.衣原体感染的免疫学:对沙眼衣原体疫苗的启示
Nat Rev Immunol. 2005 Feb;5(2):149-61. doi: 10.1038/nri1551.
5
Identification of an in vivo CD4+ T cell-mediated response to polymorphic membrane proteins of Chlamydia pneumoniae during experimental infection.实验性感染期间肺炎衣原体多态膜蛋白体内CD4 + T细胞介导反应的鉴定。
FEMS Immunol Med Microbiol. 2004 Mar 8;40(2):129-37. doi: 10.1016/S0928-8244(03)00300-6.
6
CC chemokine ligand 3 (CCL3) regulates CD8(+)-T-cell effector function and migration following viral infection.C-C趋化因子配体3(CCL3)在病毒感染后调节CD8(+) T细胞效应功能和迁移。
J Virol. 2003 Apr;77(7):4004-14. doi: 10.1128/jvi.77.7.4004-4014.2003.
7
MIP-1alpha and MIP-1beta differentially mediate mucosal and systemic adaptive immunity.巨噬细胞炎症蛋白-1α和巨噬细胞炎症蛋白-1β分别介导黏膜和全身适应性免疫。
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8
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Infect Immun. 2002 Jun;70(6):2741-51. doi: 10.1128/IAI.70.6.2741-2751.2002.
9
IFN-gamma-inducible protein 10 (CXCL10) contributes to airway hyperreactivity and airway inflammation in a mouse model of asthma.γ-干扰素诱导蛋白10(CXCL10)在哮喘小鼠模型中导致气道高反应性和气道炎症。
J Immunol. 2002 May 15;168(10):5278-86. doi: 10.4049/jimmunol.168.10.5278.
10
IFN-gamma-inducible protein 10 (IP-10; CXCL10)-deficient mice reveal a role for IP-10 in effector T cell generation and trafficking.γ干扰素诱导蛋白10(IP - 10;CXCL10)缺陷小鼠揭示了IP - 10在效应T细胞生成和运输中的作用。
J Immunol. 2002 Apr 1;168(7):3195-204. doi: 10.4049/jimmunol.168.7.3195.

沙眼衣原体肺部感染中的 1 型 T 细胞反应与局部 MIP-1alpha 反应有关。

Type 1 T-cell responses in chlamydial lung infections are associated with local MIP-1alpha response.

机构信息

Department of Immunology, Tianjin Medical University, Tianjin Key Laboratory of Cellular and Molecular Immunology, Key Laboratory of Educational Ministry of China, Tianjin, China.

出版信息

Cell Mol Immunol. 2010 Sep;7(5):355-60. doi: 10.1038/cmi.2010.32. Epub 2010 Jul 12.

DOI:10.1038/cmi.2010.32
PMID:20622889
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4002681/
Abstract

Chemokines and their receptors are important mediators of leukocyte trafficking and recruitment and sometimes work as modulators of T-cell responses during infections and inflammation. Modulating the biological activity of chemokines has been found to influence the course of diseases. However, little is known about the role of chemokine responses during chlamydial lung infections. We therefore analyzed the dynamics of multiple chemokines, which are frequently associated with type 1 (Th1) T cell immune responses, and their receptors for their expression in the lungs during Chlamydia muridarum (Cm) infections. We also examined the relationship between chemokine responses and the development of Th1 responses as well as the clearance of infection. Our results showed that in parallel with the high levels of gamma interferon (IFN-gamma) and IL-12 production in the lungs and draining lymph nodes, and the expansion of IFN-gamma-producing CD4 and CD8+ T cells, the production of the cell-related chemokines RANTES, IFN-gamma-inducible protein-10 (IP-10) and macrophage inflammatory protein-1alpha (MIP-1alpha) and their receptor CCR1 was elevated in the lung tissues after infection. Interestingly, in a later phase of infection, the expression of RANTES and IP-10 remained elevated but the expression of MIP-1alpha and CCR1 decreased to a low level, which suggests a closer association with the pattern of Th1 cytokine responses in the process of infection. These results suggest a close association between the MIP-1alpha response and the Th1-type T-cell responses in chlamydial lung infections.

摘要

趋化因子及其受体是白细胞迁移和募集的重要介质,在感染和炎症期间,有时作为 T 细胞反应的调节剂发挥作用。调节趋化因子的生物学活性被发现会影响疾病的进程。然而,人们对衣原体肺部感染期间趋化因子反应的作用知之甚少。因此,我们分析了多种趋化因子的动态,这些趋化因子通常与 1 型(Th1)T 细胞免疫反应有关,以及它们在 Chlamydia muridarum(Cm)感染期间在肺部的受体表达。我们还研究了趋化因子反应与 Th1 反应的发展以及感染清除之间的关系。我们的结果表明,与肺部和引流淋巴结中高水平的γ干扰素(IFN-γ)和 IL-12 产生以及 IFN-γ产生的 CD4 和 CD8+T 细胞扩增平行,细胞相关趋化因子 RANTES、IFN-γ诱导蛋白-10(IP-10)和巨噬细胞炎症蛋白-1α(MIP-1α)及其受体 CCR1 的产生在感染后肺部组织中升高。有趣的是,在感染的后期阶段,RANTES 和 IP-10 的表达仍然升高,但 MIP-1α 和 CCR1 的表达降低到低水平,这表明与感染过程中 Th1 细胞因子反应的模式有更密切的关联。这些结果表明,在衣原体肺部感染中,MIP-1α 反应与 Th1 型 T 细胞反应密切相关。