2012年8月24日 訊 /生物谷BIOON/ --一在動(dòng)脈粥樣硬化小鼠模型中同源抗原的存在下,，CD4+T細(xì)胞能與抗原遞呈細(xì)胞（APCs）相互作用，從而導(dǎo)致細(xì)胞的活化和增殖以及促炎性細(xì)胞因子的分泌,，這項(xiàng)最新實(shí)驗(yàn)性的研究發(fā)表在Journal of Clinical Investigation雜志上。
加利福尼亞州拉霍亞研究所過(guò)敏和免疫學(xué)醫(yī)學(xué)博士Ekaterina K. Koltsova和他的同事運(yùn)用主動(dòng)脈用活細(xì)胞成像技術(shù)比較了抗原遞呈細(xì)胞在正常以及動(dòng)脈粥樣硬化小鼠中的生物學(xué)行為和作用,。
研究人員發(fā)現(xiàn),，在同源抗原存在的情況下，CD4+T細(xì)胞能與APCs在主動(dòng)脈壁中發(fā)生的互動(dòng)，而同源抗原不存在的情況下,，兩者之間并不發(fā)生聯(lián)系,。在易發(fā)生動(dòng)脈粥樣硬化的小鼠中，APCs與主動(dòng)脈中的CD4+T細(xì)胞發(fā)生聯(lián)系后導(dǎo)致細(xì)胞的活化和增殖,，同時(shí)也促進(jìn)細(xì)胞因子（干擾素-γ,，腫瘤壞死因子-α）的分泌。
研究結(jié)論是APCs抗原遞呈給動(dòng)脈壁中的CD4+T細(xì)胞,，造成局部T細(xì)胞活化和炎性細(xì)胞因子的生產(chǎn),，從而通過(guò)慢性炎癥、誘導(dǎo)泡沫細(xì)胞的形成促進(jìn)動(dòng)脈粥樣硬化,。（生物谷：Bioon.com）
編譯自：T cells key in atherosclerosis-linked inflammation
doi:10.1172/JCI61758
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PMID:
Dynamic T cell–APC interactions sustain chronic inflammation in atherosclerosis
Ekaterina K. Koltsova1, Zacarias Garcia1, Grzegorz Chodaczek1, Michael Landau2, Sara McArdle1,3, Spencer R. Scott1, Sibylle von Vietinghoff1,4, Elena Galkina5, Yury I. Miller6, Scott T. Acton2 and Klaus Ley1
Atherosclerosis is a chronic inflammatory disease of large and medium-sized arteries characterized by leukocyte accumulation in the vessel wall. Both innate and adaptive immune responses contribute to atherogenesis, but the identity of atherosclerosis-relevant antigens and the role of antigen presentation in this disease remain poorly characterized. We developed live-cell imaging of explanted aortas to compare the behavior and role of APCs in normal and atherosclerotic mice. We found that CD4+ T cells were capable of interacting with fluorescently labeled (CD11c-YFP+) APCs in the aortic wall in the presence, but not the absence, of cognate antigen. In atherosclerosis-prone Apoe–/–CD11c-YFP+ mice, APCs extensively interacted with CD4+ T cells in the aorta, leading to cell activation and proliferation as well as secretion of IFN-γ and TNF-α. These cytokines enhanced uptake of oxidized and minimally modified LDL by macrophages. We conclude that antigen presentation by APCs to CD4+ T cells in the arterial wall causes local T cell activation and production of proinflammatory cytokines, which promote atherosclerosis by maintaining chronic inflammation and inducing foam cell formation.
