T-cell states in aortic dissection: from molecular immune profiling toward causal and translational validation.
4 affiliations
- 1Northern Jiangsu Institute of Cardiovascular Disease Prevention and Treatment, Jiangsu University, Yancheng, PR China.
- 2Department of Thoracic Surgery, Yancheng Third People's Hospital, Affiliated Hospital 6 of Nantong University, Yancheng, PR China.
- 3Medical School, Nantong University, Nantong, PR China.
- 4Department of General Medicine, Affiliated Hospital 6 of Nantong University, Yancheng Third People's Hospital, Yancheng, PR China.
Abstract
Background/objectives
Single-cell RNA sequencing and T-cell receptor profiling reveal substantial T-cell heterogeneity in aortic dissection (AD), but whether these responses contribute to vascular injury or reflect post-onset immune activation remains uncertain. This review evaluates human and experimental evidence by disease stage, tissue compartment, functional validation, T-cell specificity, and intervention timing, distinguishing descriptive profiling from evidence supporting causal and translational inference.Discussion
Human studies identify Th1/Th17-associated, CD8⁺ cytotoxicity-associated, and regulatory T-cell alterations, with stage-related differences in T-cell composition and clonality. Most evidence is cross-sectional and obtained after clinical onset. Antigen specificity, direct aortic-wall cytotoxicity, impaired Treg suppression, and T-cell-mediated aortic-wall injury remain unproven. Single-cell and TCR profiling identify candidate T-cell states and clonotypes for spatial and functional validation, not causal proof. Among candidate pathways, the IL-6-STAT3-IL-17 axis currently has the strongest AD-specific preclinical rationale, but existing interventions are largely non-T-cell-restricted and initiated before or during disease induction. Stronger causal attribution requires convergent human evidence, post-lesion T-cell-restricted perturbation, disease-progression endpoints, and rescue or target-engagement studies. The subacute phase after anatomical and haemodynamic stabilisation may offer a window to study persistent injury-amplifying T-cell responses, whereas early acute and perioperative immunomodulation remains unsupported.Conclusions
Current evidence supports altered T-cell states after AD onset but does not establish an initiating role. Near-term priorities should be prospective biomarker validation and post-lesion mechanistic studies rather than T-cell-directed immuno-modulation during the early acute and perioperative phases. Clinical translation should await reproducible associations linked to stage-specific causal mechanisms and acceptable safety.
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BibTeX
@article{ye2026tcell,
title = {{T-cell states in aortic dissection: from molecular immune profiling toward causal and translational validation.}},
author = {Xiang Ye and Yihao Wang and Yeting Li and Hao Zhu and Xia Li and Jianxiang Song},
journal = {Annals of medicine},
year = {2026},
month = oct,
doi = {10.1080/07853890.2026.2753327},
url = {https://europepmc.org/article/MED/42956058},
note = {CC BY},
}
RIS
TY - JOUR
TI - T-cell states in aortic dissection: from molecular immune profiling toward causal and translational validation.
AU - Xiang Ye
AU - Yihao Wang
AU - Yeting Li
AU - Hao Zhu
AU - Xia Li
AU - Jianxiang Song
PY - 2026
DA - 2026/10/29
JO - Annals of medicine
DO - 10.1080/07853890.2026.2753327
UR - https://europepmc.org/article/MED/42956058
AB - Background/objectives Single-cell RNA sequencing and T-cell receptor profiling reveal substantial T-cell heterogeneity in aortic dissection (AD), but whether these responses contribute to vascular injury or reflect post-onset immune activation remains uncertain. This review evaluates human and experimental evidence by disease stage, tissue compartment, functional validation, T-cell specificity, and intervention timing, distinguishing descriptive profiling from evidence supporting causal and translational inference.Discussion Human studies identify Th1/Th17-associated, CD8⁺ cytotoxicity-associated, and regulatory T-cell alterations, with stage-related differences in T-cell composition and clonality. Most evidence is cross-sectional and obtained after clinical onset. Antigen specificity, direct aortic-wall cytotoxicity, impaired Treg suppression, and T-cell-mediated aortic-wall injury remain unproven. Single-cell and TCR profiling identify candidate T-cell states and clonotypes for spatial and functional validation, not causal proof. Among candidate pathways, the IL-6-STAT3-IL-17 axis currently has the strongest AD-specific preclinical rationale, but existing interventions are largely non-T-cell-restricted and initiated before or during disease induction. Stronger causal attribution requires convergent human evidence, post-lesion T-cell-restricted perturbation, disease-progression endpoints, and rescue or target-engagement studies. The subacute phase after anatomical and haemodynamic stabilisation may offer a window to study persistent injury-amplifying T-cell responses, whereas early acute and perioperative immunomodulation remains unsupported.Conclusions Current evidence supports altered T-cell states after AD onset but does not establish an initiating role. Near-term priorities should be prospective biomarker validation and post-lesion mechanistic studies rather than T-cell-directed immuno-modulation during the early acute and perioperative phases. Clinical translation should await reproducible associations linked to stage-specific causal mechanisms and acceptable safety.
SN - 0785-3890
SN - 1365-2060
ER -