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血液CD4+ T细胞表型与功能和胸段升主动脉瘤的关系：一项实验研究。

Relationships Between Phenotype and Function of Blood CD4+ T-Cells and Ascending Thoracic Aortic Aneurysm: an Experimental Study.

作者信息

Sbrana Silverio, Tiwari Kaushal Kishore, Bevilacqua Stefano, Giungato Paola, Kallushi Enkel, Solinas Marco, Mazzone Anna Maria

机构信息

Flow Cytometry Laboratory, CNR Institute of Clinical Physiology, Massa, Italy.

Cardiac Surgery Department "G. Pasquinucci" Heart Hospital, "G. Monasterio" Foundation, Massa, Italy.

出版信息

Braz J Cardiovasc Surg. 2019 Jan-Feb;34(1):8-16. doi: 10.21470/1678-9741-2018-0310.

DOI:10.21470/1678-9741-2018-0310
PMID:30810667
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6385830/
Abstract

INTRODUCTION

Non-familial ascending thoracic aorta dilation and aneurysms (TAAs) are silent diseases in elderly patients. Histopathology revealed that functionally polarized infiltrating CD4+ T-cells play a key role in aortic wall weakening.

OBJECTIVE

To evaluate the possible associations between phenotype and cytokine production of circulating CD4+ T-lymphocytes and the presence of TAA in patients with aortic valve disease (AVD).

METHODS

We studied blood samples from 10 patients with TAA and 10 patients with AVD. Flow cytometry was used to quantify: a) CD4+ T-lymphocytes surface expression of CD25, CD28, and chemokine receptors (CCR5, CXCR3, CX3CR1); b) fractions of in vitro stimulated CD4+ T-cells producing cytokines (interferon gamma [IFN-γ], interleukin [IL]-17A, IL-21, IL-10); c) CD4+CD25highFoxP3+ regulatory T-cells (Treg) fraction. Enzyme-linked immunosorbent assays (ELISA) were performed for cytokines (IFN-γ, IL-6, IL-10, IL-17A, IL-23, transforming growth factor beta [TGF-β]) and chemokines (RANTES, CX3CL1).

RESULTS

The total CD4+CD28±CD4+/CX3CR1+ T-cells fraction was higher (P=0.0323) in AVD (20.452±4.673) than in TAA patients (8.633±2.030). The frequency ratio of CD4+ T-lymphocytes producing IFN-γ vs. IL-17A+IL-21 cytokine-producing CD4+ T-cells was higher (P=0.0239) in AVD (2.102±0.272) than in TAA (1.365±0.123) patients. The sum of CD4+CD28±CD4+/CX3CR1+ T-cells correlated positively with values of the previous cytokine ratio (P=0.0002, R=0.732). The ratio of CD4+CD28±CD4+/CX3CR1+ T-cells vs. Treg was higher (P=0.0008) in AVD (20.859±3.393) than in TAA (6.367±1.277) patients.

CONCLUSION

Our results show that the presence of TAA in subjects with AVD is associated with imbalance between phenotypic and cytokine-producing subsets of circulating CD4+ T-lymphocytes, prevalently oriented towards a pro-fibrotic and IFN-γ counteracting effect to functional polarization.

摘要

引言

非家族性升主动脉扩张和动脉瘤（TAAs）在老年患者中是隐匿性疾病。组织病理学显示，功能极化的浸润性CD4 + T细胞在主动脉壁弱化中起关键作用。

目的

评估主动脉瓣疾病（AVD）患者循环CD4 + T淋巴细胞的表型和细胞因子产生与TAAs存在之间的可能关联。

方法

我们研究了10例TAAs患者和10例AVD患者的血样。采用流式细胞术定量分析：a）CD4 + T淋巴细胞表面CD25、CD28和趋化因子受体（CCR5、CXCR3、CX3CR1）的表达；b）体外刺激产生细胞因子（干扰素γ [IFN-γ]、白细胞介素 [IL]-17A、IL-21、IL-10）的CD4 + T细胞比例；c）CD4 + CD25highFoxP3 +调节性T细胞（Treg）比例。采用酶联免疫吸附测定（ELISA）检测细胞因子（IFN-γ、IL-6、IL-10、IL-17A、IL-23、转化生长因子β [TGF-β]）和趋化因子（RANTES、CX3CL1）。

结果

AVD患者（20.452±4.673）的总CD4 + CD28±CD4 + /CX3CR1 + T细胞比例高于TAAs患者（8.633±2.030）（P = 0.0323）。AVD患者（2.102±0.272）中产生IFN-γ的CD4 + T淋巴细胞与产生IL-17A + IL-21细胞因子的CD4 + T细胞的频率比高于TAAs患者（1.365±0.123）（P = 0.0239）。CD4 + CD28±CD4 + /CX3CR1 + T细胞总数与先前细胞因子比例值呈正相关（P = 0.0002，R = 0.732）。AVD患者（20.859±3.393）的CD4 + CD28±CD4 + /CX3CR1 + T细胞与Treg的比例高于TAAs患者（6.367±1.277）（P = 0.0008）。

结论

我们的结果表明，AVD患者中TAAs的存在与循环CD4 + T淋巴细胞表型和产生细胞因子亚群之间的失衡有关，这种失衡主要倾向于促纤维化和对功能极化的IFN-γ拮抗作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/290d/6385830/a88441485c78/rbccv-34-01-0008-g06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/290d/6385830/36f23d8bb704/rbccv-34-01-0008-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/290d/6385830/ce828bdcc4ea/rbccv-34-01-0008-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/290d/6385830/054d3a3d787a/rbccv-34-01-0008-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/290d/6385830/27f2f5284d82/rbccv-34-01-0008-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/290d/6385830/7a860be6a151/rbccv-34-01-0008-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/290d/6385830/a88441485c78/rbccv-34-01-0008-g06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/290d/6385830/36f23d8bb704/rbccv-34-01-0008-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/290d/6385830/ce828bdcc4ea/rbccv-34-01-0008-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/290d/6385830/054d3a3d787a/rbccv-34-01-0008-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/290d/6385830/27f2f5284d82/rbccv-34-01-0008-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/290d/6385830/7a860be6a151/rbccv-34-01-0008-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/290d/6385830/a88441485c78/rbccv-34-01-0008-g06.jpg

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