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非免疫细胞在对克氏锥虫感染的固有免疫反应中促成免疫细胞与炎症介质之间的相互作用。

Nonimmune Cells Contribute to Crosstalk between Immune Cells and Inflammatory Mediators in the Innate Response to Trypanosoma cruzi Infection.

作者信息

Aoki Maria Pilar, Carrera-Silva Eugenio Antonio, Cuervo Henar, Fresno Manuel, Gironès Núria, Gea Susana

机构信息

Departamento de Bioquímica Clínica, Centro de Investigaciones en Bioquímica Clínica e Inmunología (CIBICI), Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Facultad de Ciencias Químicas, Universidad Nacional de Córdoba, Córdoba 5000, Argentina.

出版信息

J Parasitol Res. 2012;2012:737324. doi: 10.1155/2012/737324. Epub 2011 Aug 18.

DOI:10.1155/2012/737324
PMID:21869919
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3159004/
Abstract

Chagas myocarditis, which is caused by infection with the intracellular parasite Trypanosoma cruzi, remains the major infectious heart disease worldwide. Innate recognition through toll-like receptors (TLRs) on immune cells has not only been revealed to be critical for defense against T. cruzi but has also been involved in triggering the pathology. Subsequent studies revealed that this parasite activates nucleotide-binding oligomerization domain- (NOD-)like receptors and several particular transcription factors in TLR-independent manner. In addition to professional immune cells, T. cruzi infects and resides in different parenchyma cells. The innate receptors in nonimmune target tissues could also have an impact on host response. Thus, the outcome of the myocarditis or the inflamed liver relies on an intricate network of inflammatory mediators and signals given by immune and nonimmune cells. In this paper, we discuss the evidence of innate immunity to the parasite developed by the host, with emphasis on the crosstalk between immune and nonimmune cell responses.

摘要

恰加斯心肌炎由细胞内寄生虫克氏锥虫感染引起,仍是全球主要的感染性心脏病。免疫细胞上的Toll样受体(TLR)介导的固有识别不仅对抵御克氏锥虫至关重要,还参与引发病理过程。后续研究表明,这种寄生虫以不依赖TLR的方式激活核苷酸结合寡聚化结构域(NOD)样受体和几种特定转录因子。除了专职免疫细胞外,克氏锥虫还感染并寄生于不同的实质细胞。非免疫靶组织中的固有受体也可能影响宿主反应。因此,心肌炎或炎症性肝病的转归取决于免疫细胞和非免疫细胞发出的复杂炎症介质和信号网络。在本文中,我们讨论宿主针对该寄生虫产生的固有免疫证据,重点关注免疫细胞和非免疫细胞反应之间的相互作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4cfa/3159004/3edf451a3249/JPR2012-737324.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4cfa/3159004/192a8b7831ae/JPR2012-737324.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4cfa/3159004/c373af8ee0f6/JPR2012-737324.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4cfa/3159004/3edf451a3249/JPR2012-737324.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4cfa/3159004/192a8b7831ae/JPR2012-737324.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4cfa/3159004/c373af8ee0f6/JPR2012-737324.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4cfa/3159004/3edf451a3249/JPR2012-737324.003.jpg

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