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首页> 外文期刊>Current opinion in lipidology >T cells in arteritis and atherosclerosis.
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T cells in arteritis and atherosclerosis.

机译：T细胞在动脉炎和动脉粥样硬化中。

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PURPOSE OF REVIEW: Inflammatory vasculopathies, spanning from atherosclerosis to vasculitides, are driven by innate and adaptive immune responses. Instructed by antigen-presenting cells, T cells have unsurpassed skills to orchestrate protective and pathogenic immunity. Pro-inflammatory and anti-inflammatory T cells regulate master pathogenic pathways, providing a framework for novel immunotherapeutic strategies. RECENT FINDINGS: The multilayered wall of macrovessels creates a unique tissue niche; professional antigen-presenting cells, specifically dendritic cells, are superior in triggering and maintaining T-cell responses in this tissue milieu. Plaque-residing dendritic cells sense pathogen-derived motifs and edit inflammatory responses. T cells respond to antigen but antigen-nonspecific factors setting cellular response thresholds may be equally important. Dysregulated signal transduction pathways emerge as highly relevant in biasing T cells toward hyperresponsiveness. In the inflamed atheroma and inarteritic lesions, pathogenic T cells coordinate multiple injury pathways. Besides inducing tissue-damaging macrophage functions, they directly inflict cellular injury within the arterial wall. Distinctively, selected T cells induce smooth muscle cell apoptosis, most prominently by upregulating the death-receptor ligand TRAIL. SUMMARY: Innate sentinels, specifically dendritic cells, populate normal arteries, intramural vasculitic lesions, and the inflamed atheroma. They sense microbial motifs and instruct T cells toward pro-inflammatory and tissue-destructive effector functions. Microenvironmental factors imposed by the unique structure of the arterial wall appear to be highly conserved across disease entities, modulating inflammation in atherosclerosis and arteritis.
机译：审查目的：从动脉粥样硬化到血管炎的炎性血管病变由先天性和适应性免疫反应驱动。在抗原呈递细胞的指导下，T细胞具有无与伦比的协调保护性和致病性免疫的技能。促炎性和抗炎性T细胞调节主要的致病途径，为新型免疫治疗策略提供了框架。最近的发现：巨血管的多层壁创造了独特的组织生态位。专业的抗原呈递细胞，特别是树突状细胞，在触发和维持该组织环境中的T细胞反应方面表现优异。斑块状树突状细胞感知病原体衍生的基序并编辑炎症反应。 T细胞对抗原有反应，但设定细胞反应阈值的非抗原非抗原因素可能同样重要。失调的信号转导途径与使T细胞偏向高反应性高度相关。在发炎的动脉粥样硬化和动脉病变中，致病性T细胞可协调多种损伤途径。除了诱导破坏组织的巨噬细胞功能外，它们还直接在动脉壁内造成细胞损伤。独特地，选定的T细胞通过上调死亡受体配体TRAIL最明显地诱导平滑肌细胞凋亡。摘要：先天性前哨，特别是树突状细胞，分布于正常动脉，壁内血管病变和发炎的动脉粥样硬化。他们感知微生物的基序，并指导T细胞实现促炎和破坏组织的效应器功能。由动脉壁的独特结构所施加的微环境因素似乎在各个疾病实体中都是高度保守的，从而调节了动脉粥样硬化和动脉炎中的炎症。

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