Category Ranking
98%
Total Visits
921
Avg Visit Duration
2 minutes
Citations
20
Article Abstract
The heart is an autoimmune-prone organ. It is crucial for the heart to keep injury-induced autoimmunity in check to avoid autoimmune-mediated inflammatory disease. However, little is known about how injury-induced autoimmunity is constrained in hearts. Here, we reveal an unknown intramyocardial immunosuppressive program driven by Tbx1, a DiGeorge syndrome disease gene that encodes a T-box transcription factor (TF). We found induced profound lymphangiogenic and immunomodulatory gene expression changes in lymphatic endothelial cells (LECs) after myocardial infarction (MI). The activated LECs penetrated the infarcted area and functioned as intramyocardial immune hubs to increase the numbers of tolerogenic dendritic cells (tDCs) and regulatory T (Treg) cells through the chemokine Ccl21 and integrin Icam1, thereby inhibiting the expansion of autoreactive CD8 T cells and promoting reparative macrophage expansion to facilitate post-MI repair. Mimicking its timing and implementation may be an additional approach to treating autoimmunity-mediated cardiac diseases.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.immuni.2023.07.019 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Organelle stresses and energetic metabolisms promote endothelial-to-mesenchymal transition and fibrosis via upregulating FOSB and MEOX1 in Alzheimer's disease.
Front Mol Neurosci
August 2025
Department of Cardiovascular Sciences, Lewis Katz School of Medicine, Lemole Center for Integrated Lymphatics and Vascular Research, Temple University, Philadelphia, PA, United States.
Introduction: Endothelial-to-mesenchymal transition (EndoMT), cell death, and fibrosis are increasingly recognized as contributing factors to Alzheimer's disease (AD) pathology, but the underlying transcriptomic mechanisms remain poorly defined. This study aims to elucidate transcriptomic changes associated with EndoMT, diverse cell death pathways, and fibrosis in AD using the 3xTg-AD mouse model.
Methods: Using RNA-seq data and knowledge-based transcriptomic analysis on brain tissues from the 3xTg-AD mouse model of AD.
NO-Driven Janus Nanomotor Enhances T-Cell Infiltration by Reconstructing Tumor-Associated Blood and Lymphatic Vessels.
Adv Sci (Weinh)
September 2025
Department of Pharmaceutics, Shandong Key Laboratory of Targeted Drug Delivery and Advanced Pharmaceutics, NMPA Key Laboratory for Technology Research and Evaluation of Drug Products, Key Laboratory of Chemical Biology (Ministry of Education), State Key Laboratory of Discovery and Utilization of Fun
The effectiveness of antitumor immunotherapy is limited to immune cell infiltration into solid tumors, primarily via T-cell migration through tumor blood vessels. This study introduces a multifunctional nitric oxide (NO)-driven hollow gold Janus nanomotor (HAM) designed to promote tumor blood vessel normalization and increase T-cell infiltration, thereby enhancing the immune response against tumors. It is revealed that self-generated NO facilitates the penetration of HAM into tumors and increases pericyte coverage of blood vessels, thereby enhancing intratumoral T-cell infiltration.
View Article and Find Full Text PDFDecoding coal-induced pulmonary endothelial injury using single-cell omics.
Ecotoxicol Environ Saf
September 2025
School of Public Health, Anhui University of Science and Technology, Huainan, China; Key Laboratory of Industrial Dust Control and Occupational Health of the Ministry of Education, Anhui University of Science and Technology, Huainan, China; Key Laboratory of Industrial Dust Deep Reduction and Occupa
Pulmonary endothelial injury is a critical factor in the pathogenesis and progression of coal pneumoconiosis. However, the precise mechanisms underlying this injury remain poorly understood. To address this, we established a coal pneumoconiosis mouse model by chronic intranasal coal dust exposure over 9 months.
View Article and Find Full Text PDFProgrammed cell death-driven remodeling of the melanoma microenvironment enables prognostic stratification and therapeutic prediction.
Front Immunol
September 2025
Wound Healing Center, Peking University Third Hospital, Beijing, China.
Background And Objective: Melanoma exhibits profound biological complexity, driven by immune evasion, phenotypic plasticity, and resistance to therapy. While programmed cell death (PCD) shapes tumor-immune interactions, its mechanistic landscape in melanoma remains incompletely defined. This study aims to comprehensively characterize PCD-related signatures and their associations with tumor heterogeneity, prognosis, and immunotherapeutic outcomes.
View Article and Find Full Text PDFEnhanced meningeal lymphatic drainage alleviates cognitive dysfunction induced by anesthesia and surgery in aged mice.
Neuropharmacology
September 2025
Department of Anesthesiology, Hebei Medical University Third Hospital, Shijiazhuang, 050051, Hebei Province, PR China. Electronic address:
Postoperative cognitive dysfunction (POCD) occurs in elderly surgical patients as a common complication and manifests as cognitive decline. It is associated with neuroinflammation, microglial activation, and impaired metabolic waste clearance-key mechanisms underlying POCD. Meningeal lymphatic vessels (MLVs) facilitate the drainage of cerebrospinal fluid (CSF) and interstitial fluid (IF), regulating brain immune responses and clearing metabolic waste, immune cells, and antigens, thus modulating neuroinflammation.
View Article and Find Full Text PDF