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腹主动脉瘤患者 CD4 T 细胞亚群的特征。

Characterization of CD4 T Cell Subsets in Patients with Abdominal Aortic Aneurysms.

机构信息

Department of Clinical Pathology, Faculty of Medical Sciences, State University of Campinas (UNICAMP), Campinas, São Paulo 13083-887, Brazil.

Faculty of Medicine of Jundiai, Jundiai, São Paulo 13202-550, Brazil.

出版信息

Mediators Inflamm. 2018 Dec 27;2018:6967310. doi: 10.1155/2018/6967310. eCollection 2018.

DOI:10.1155/2018/6967310
PMID:30686933
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6327259/
Abstract

BACKGROUND

The mediators produced by CD4 T lymphocytes are involved in the pathogenesis of aneurysmal lesions in abdominal aortic aneurysm (AAA) patients. The aim of this study was to identify and characterize the CD4 T cell subsets involved in human AAA.

METHODS

The CD4 T cell subsets in 30 human aneurysmal lesions were determined using flow cytometry (FC) and immunohistochemistry (IHC). The peripheral blood mononuclear cells (PBMCs) from patients with AAA were also analyzed by FC and compared with control subjects.

RESULTS

Human aneurysmal lesions contained IFN-, IL-12p35, IL-4, IL-23p19, IL-17R, and IL-22 positive cells. PBMCs from AAA patients had higher expression levels of IFN-, TNF-, IL-4, and IL-22 when compared to controls.

CONCLUSIONS

Our results show the presence of T1, T2, T17, and T22 subsets in aneurysmal lesions of AAA patients and suggest that these cells may be mainly activated in situ, where they can induce tissue degradation and contribute to the pathogenesis of AAA.

摘要

背景

CD4 T 淋巴细胞产生的介质参与了腹主动脉瘤(AAA)患者动脉瘤病变的发病机制。本研究旨在鉴定和描述参与人类 AAA 的 CD4 T 细胞亚群。

方法

通过流式细胞术(FC)和免疫组织化学(IHC)确定 30 个人类动脉瘤病变中的 CD4 T 细胞亚群。还通过 FC 分析 AAA 患者的外周血单核细胞(PBMC),并与对照进行比较。

结果

人类动脉瘤病变中含有 IFN-、IL-12p35、IL-4、IL-23p19、IL-17R 和 IL-22 阳性细胞。与对照组相比,AAA 患者的 PBMC 中 IFN-、TNF-、IL-4 和 IL-22 的表达水平更高。

结论

我们的结果表明,AAA 患者的动脉瘤病变中存在 T1、T2、T17 和 T22 亚群,提示这些细胞可能主要在原位激活,在原位诱导组织降解并有助于 AAA 的发病机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e86/6327259/d1068077b6fb/MI2018-6967310.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e86/6327259/a14c21403d5c/MI2018-6967310.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e86/6327259/1fbc1507138c/MI2018-6967310.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e86/6327259/7e57e03aa38b/MI2018-6967310.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e86/6327259/d1068077b6fb/MI2018-6967310.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e86/6327259/a14c21403d5c/MI2018-6967310.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e86/6327259/1fbc1507138c/MI2018-6967310.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e86/6327259/7e57e03aa38b/MI2018-6967310.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e86/6327259/d1068077b6fb/MI2018-6967310.004.jpg

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