Abstract

BackgroundProgressive dilatation is responsible for significant mortality and morbidity in patients with thoracic aortic aneurysms (TAAs). Studies have shown that the development and progression of TAAs are closely related to immune regulatory pathways and genes. Therefore, it is important to understand the immune regulatory mechanisms and biomarkers of TAA dilatation.MethodsSystematic bioinformatics analysis was applied, including linear models for microarray data (LIMMA) differential expression analyses, principal component analysis (PCA), immunocyte identification, and genetic function enrichment analysis.ResultsOur results showed that both aortic intima-media (AMed) and outer aortic adventitia (AAdv) tissues were closely associated with T cell activation during the process of tricuspid aortic valve (TAV)-associated TAA dilation. Additionally, the degree of infiltration of resting memory CD4+ T cells was linked to both AAdv and AMed vascular dilation. The core regulators PPTRC, IL1B, CD4, CD3G, and IL2RA were also identified and are closely related to resting memory CD4+ T cell infiltration in this pathological process.ConclusionsThe candidate genes PPTRC, IL1B, CD4, CD3G, and IL2RA were involved in the regulation of resting memory CD4 T cell tissue infiltration, which is closely related to the process of AAdv and AMed vascular dilation in TAV patients.

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