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MINI REVIEW article
Front. Immunol.
Sec. Vaccines and Molecular Therapeutics
Volume 16 - 2025 |
doi: 10.3389/fimmu.2025.1547213
This article is part of the Research Topic Innovative Adjuvant Strategies: Enhancing Vaccine Efficacy Through Transdisciplinary Approaches View all articles
Harnessing Adjuvant-Induced Epigenetic Modulation for Enhanced Immunity in Vaccines and Cancer Therapy
Provisionally accepted- Center for Vaccine Development, University of Maryland, Baltimore, United States
Adjuvants are crucial in vaccines and cancer therapies, enhancing therapeutic efficacy through diverse mechanisms. In vaccines, adjuvants are traditionally valued for amplifying immune responses, ensuring robust and long-lasting protection against pathogens. In cancer treatments, adjuvants can boost the effectiveness of chemotherapy or immunotherapy by targeting tumor antigens, rendering cancer cells more vulnerable to treatment. Recent research has uncovered new molecular-level effects of the adjuvants, mainly through epigenetic mechanisms. Epigenetics encompasses heritable modifications in gene expression that do not alter the DNA sequence, impacting processes such as DNA methylation, histone modification, and non-coding RNA expression. These epigenetic changes play a pivotal role in regulating gene activity, influencing immune pathways, and modulating the strength and duration of immune responses. Whether in vaccines or cancer treatments, understanding how adjuvants interact with epigenetic regulators offers significant potential for developing more precise, cell-targeted therapies across various medical fields. This review delves into the evolving role of adjuvants and their interactions with epigenetic mechanisms. It also examines the potential of harnessing epigenetic changes to enhance adjuvant efficacy and explores the novel use of epigenetic inhibitors as adjuvants in therapeutic settings.
Keywords: Adjuvant, epigenetic, vaccine, cancer therapy NLRP3, NOD-like receptor protein 3, PLGA, polymers like poly(lactic-co-glycolic) acid, NF-κB, nuclear factor kappa-B, TLR, toll-like receptors, IRF, interferon regulatory factor, DC, dendritic cell, TF, transcription factor, STAT, signal transducer and activator of transcription
Received: 17 Dec 2024; Accepted: 05 Feb 2025.
Copyright: © 2025 Megdiche and Salerno-Goncalves. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
Rosangela Salerno-Goncalves, Center for Vaccine Development, University of Maryland, Baltimore, United States
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