CD11c+细胞的缺失减缓了腹主动脉瘤的进展。

Keisuke Okuno, Stephanie Cicalese, Satoru Eguchi
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引用次数: 1

摘要

动脉壁的慢性炎症与腹主动脉瘤(AAA)的发展有关。然而,炎症细胞参与AAA发病机制的详细分子机制在很大程度上仍不清楚。Krishna等人在《临床科学》杂志上发表的文章中报道,CD11c+树突状细胞的耗损抑制了小鼠实验性AAA的形成。作者还证明了循环中CD4和CD8阳性T细胞减少,血浆中性粒细胞弹性酶活性降低,主动脉基质重塑。这些新发现将有助于阐明AAA进展的潜在机制,并可能为未来AAA形成的治疗研究提供新的靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Depletion of CD11c+ cell attenuates progression of abdominal aortic aneurysm.

Chronic inflammation of the arterial wall has been implicated in the development of abdominal aortic aneurysm (AAA). However, the detailed molecular mechanism(s) by which inflammatory cells contributes to AAA pathogenesis remains largely unclear. In their article in Clinical Science, Krishna et al. have reported that depletion of CD11c+ dendritic cells inhibited experimental AAA formation in mice. The authors also demonstrated a decrease in CD4 and CD8 positive T cells in the circulation, lower plasma neutrophil elastase activity, and aortic matrix remodeling. These novel findings will help clarify the underlying mechanisms of AAA progression and may provide a new target for future therapeutic research in AAA formation.

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