脂氧素作为一种免疫逃避机制。

Lipoxins as an immune-escape mechanism.

机构信息

Division of Molecular Immunology, Cincinnati Children's Hospital Medical Center and University of Cincinnati College of Medicine, Cincinnati, Ohio 45229, USA.

出版信息

Adv Exp Med Biol. 2009;666:78-87. doi: 10.1007/978-1-4419-1601-3_6.

DOI:10.1007/978-1-4419-1601-3_6

PMID:20054976

Abstract

Here, we discuss the mechanisms of repression of signaling pathways that are triggered by Lipoxin (LX) and are responsible for control of pro-inflammatory response during chronic phase of Toxoplasma gondii infection. We also discuss this mechanism from the perspective of the pathogen, which pirates the host's lipoxygenase machinery to its own advantage as a probable immune-escape mechanism. Pro-inflammatory mediators such as IL-12, IFN-gamma and TNF are essential in controlling parasite growth during T. gondii infection. However, it is clear that exacerbated production of these cytokines results in host tissue damage. LX, an anti-inflammatory eicosanoid, plays an important role in regulation of immune response to T. gondii.

摘要

在这里，我们讨论了脂氧素（LX）触发的信号通路被抑制的机制，这些信号通路负责控制弓形虫感染慢性期的促炎反应。我们还从病原体的角度讨论了这一机制，病原体利用宿主的脂氧合酶机制为自身谋取利益，这可能是一种免疫逃避机制。在弓形虫感染过程中，促炎介质如 IL-12、IFN-γ和 TNF 对于控制寄生虫的生长是必不可少的。然而，很明显，这些细胞因子的过度产生会导致宿主组织损伤。LX 是一种抗炎类二十烷，在调节对弓形虫的免疫反应中发挥重要作用。