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Trained immunity is a renewed concept of innate immune memory that facilitates the innate immune system to have the capacity to remember and train cells via metabolic and transcriptional events to enable them to provide nonspecific defense against the subsequent encounters with a range of pathogens and acquire a quicker and more robust immune response, but different from the adaptive immune memory. Reversing the epigenetic changes or targeting the immunological pathways may be considered potential therapeutic approaches to counteract the hyper-responsive or hypo-responsive state of trained immunity. The efficient regulation of immune homeostasis and promotion or inhibition of immune responses is required for a balanced response. Trained immunity-based vaccines can serve as potent immune stimuli and help in the clearance of pathogens in the body through multiple or heterologous effects and confer protection against nonspecific and specific pathogens. This review highlights various features of trained immunity and its applications in developing novel therapeutics and vaccines, along with certain detrimental effects, challenges as well as future perspectives.
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http://dx.doi.org/10.1080/21645515.2022.2040238 | DOI Listing |
Front Immunol
August 2025
Immunobiology Group, International Centre for Genetic Engineering and Biotechnology, New Delhi, India.
[This corrects the article DOI: 10.3389/fimmu.2025.
View Article and Find Full Text PDFCell Immunol
September 2025
Shaanxi Key Laboratory of Agricultural and Environmental Microbiology, College of Life Sciences, Northwest A&F University, Yangling, Shaanxi 712100, China. Electronic address:
Both trained immunity (TRIM) and endotoxin tolerance (ET) initiate similar metabolic reprogramming characterized by enhanced glycolysis following an initial stimulus. However, TRIM exhibited heightened immune activation upon restimulation, whereas ET showed suppressed innate immune response. This divergence is attributed to distinct metabolic intermediates accumulated after the initial stimulation.
View Article and Find Full Text PDFCardiovasc Res
September 2025
Center for Cardiovascular Research, Division of Cardiology, Department of Medicine, Washington University in Saint Louis, St. Louis, MO, USA.
Aims: Although the ability of the heart to adapt to environmental stress has been studied extensively, the molecular and cellular mechanisms responsible for cardioprotection are not yet fully understood. In this study, we sought to elucidate these mechanisms for cytoprotection using a model of stress-induced cardiomyopathy.
Methods And Results: We administered Toll-like receptor (TLR) agonists or diluent to wild-type mice and assessed for cardioprotection against injury from a high intraperitoneal dose of isoproterenol (ISO) administered 7 days later.
Elife
September 2025
State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, Guangzhou, China.
Innate immune cells can acquire a memory phenotype, termed trained immunity, but the mechanism underlying the regulation of trained immunity remains largely elusive. Here, we demonstrate that inhibition of Aurora kinase A (AurA) dampens trained immunity induced by β-glucan. ATAC-seq and RNA-seq analysis reveal that AurA inhibition restricts chromatin accessibility of genes associated with inflammatory pathways such as JAK-STAT, TNF, and NF-κB pathways.
View Article and Find Full Text PDFTransplant Direct
September 2025
Unidad Transplante de О́rganos, Centro Nacional de Microbiología, Instituto de Salud Carlos III, Madrid, Spain.
Extracorporeal photopheresis (ECP) is a well-established, safe, and effective immunomodulatory therapy currently used in clinics to decrease T cell-mediated immunity in various disorders, including autoimmune diseases and chronic rejection in organ transplantation. Although the ECP procedure has been shown to induce apoptotic cells that are reintroduced into the patient at the end of the treatment, the precise tolerogenic mechanisms mediated by ECP are not fully understood. Previous in vitro studies have demonstrated that early apoptotic cells express annexins on their cell surface, which suppress myeloid cell activation on stimulation with bacterial lipopolysaccharide through Toll-like receptors.
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