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诱导性长QT综合征的非衰竭心脏供体免疫谱改变：心脏移植血管病变的潜在危险因素。

Altered Immune Profiles in Non-Failing Heart Donors With Induced Long QT Syndrome: A Potential Risk Factor for Cardiac Allograft Vasculopathy.

作者信息

Wen Zhi, Shao Shuai, Feng Yu, Wang Zheng, Wu Jianqiang, Wu Changxue, Tian Mingwu

机构信息

Department of Cardiothoracic Vascular Surgery, People's Hospital of Deyang City, Deyang, Sichuan, P.R. China.

College of Pharmacy, The Ohio State University, Columbus, Ohio, USA.

出版信息

Clin Transplant. 2025 Aug;39(8):e70286. doi: 10.1111/ctr.70286.

DOI:10.1111/ctr.70286
PMID:40844500
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12372863/
Abstract

INTRODUCTION

Cardiac allograft vasculopathy (CAV) develops more aggressively in recipients of hearts from brain-dead (BD) donors with induced long QT syndrome (iLQTS), yet the underlying mechanisms remain poorly understood. In this study, we employ a multi-omics and experimental framework to explore the role of neuro-immune interactions in non-failing donor hearts affected by iLQTS.

METHODS

Single-nuclei RNA sequencing (snRNA-seq) compared four iLQTS and four non-arrhythmic non-failing donor hearts. Pathway enrichment and cell-cell communication were assessed. Plasma proteome data from BD donors and neuronal differentially expressed (DE) genes were integrated via Omicsnet. Human BD donor transcriptomes data were analyzed for immune correlation.

RESULTS

ILQTS hearts showed elevated T/mast cells and upregulated leukocyte migration/focal adhesion pathways. Neuronal signaling (NGF, HSPG) and adhesion molecules (ITGB1, LAMININ) drove immune trafficking. Integrative proteomics identified ITGB1 as a central hub linking neuronal DE genes to BD-associated plasma proteins. Human validation linked activated CD4 T cells/Th2 enrichment to prolonged QT intervals.

CONCLUSIONS

Neuro-immune dysregulation and integrin signaling related T cell activation underlie iLQTS-related heart donors. Targeting neuronal-integrin crosstalk may reduce CAV progression and improve transplant outcomes.

摘要

引言

在患有诱发性长QT综合征（iLQTS）的脑死亡（BD）供体心脏的接受者中，心脏移植血管病变（CAV）发展更为迅猛，但其潜在机制仍知之甚少。在本研究中，我们采用多组学和实验框架来探究神经免疫相互作用在受iLQTS影响的非衰竭供体心脏中的作用。

方法

单核RNA测序（snRNA-seq）比较了四个iLQTS供体心脏和四个无心律失常的非衰竭供体心脏。评估了通路富集和细胞间通讯。通过Omicsnet整合了来自BD供体的血浆蛋白质组数据和神经元差异表达（DE）基因。分析了人类BD供体转录组数据的免疫相关性。

结果

iLQTS心脏显示T/肥大细胞升高，白细胞迁移/粘着斑通路上调。神经元信号传导（NGF、HSPG）和粘附分子（ITGB1、层粘连蛋白）驱动免疫运输。整合蛋白质组学确定ITGB1是将神经元DE基因与BD相关血浆蛋白联系起来的中心枢纽。人体验证将活化的CD4 T细胞/Th2富集与QT间期延长联系起来。

结论

神经免疫失调和整合素信号传导相关的T细胞活化是iLQTS相关心脏供体的基础。靶向神经元-整合素串扰可能会减少CAV进展并改善移植结果。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b4d/12372863/8d35f65ce2cd/CTR-39-e70286-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b4d/12372863/0826b8f45805/CTR-39-e70286-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b4d/12372863/11114dc42ffe/CTR-39-e70286-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b4d/12372863/9ec45fe692ad/CTR-39-e70286-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b4d/12372863/8d35f65ce2cd/CTR-39-e70286-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b4d/12372863/0826b8f45805/CTR-39-e70286-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b4d/12372863/11114dc42ffe/CTR-39-e70286-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b4d/12372863/9ec45fe692ad/CTR-39-e70286-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b4d/12372863/8d35f65ce2cd/CTR-39-e70286-g001.jpg

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本文引用的文献

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Donor Electrocardiogram Associations With Cardiac Dysfunction, Heart Transplant Use, and Survival: The Donor Heart Study.供体心电图与心功能障碍、心脏移植使用和生存的关系：供心研究。
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Inverted direct allorecognition triggers early donor-specific antibody responses after transplantation.
移植后，反向直接同种异体识别会引发早期的供体特异性抗体反应。
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