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REVIEW article

Front. Immunol.

Sec. Inflammation

Volume 16 - 2025 | doi: 10.3389/fimmu.2025.1523503

This article is part of the Research Topic Post-Transcriptional Modifications in Cancer Immunity and Immunotherapy View all 4 articles

Methyltransferase-like 3-mediated RNA N 6 -methyladenosine contributes to immune dysregulation: diagnostic biomarker and therapeutic target

Provisionally accepted
  • 1 West China Second University Hospital, Sichuan University, Chengdu, China
  • 2 Chengdu Medical College, Chengdu, Sichuan, China

The final, formatted version of the article will be published soon.

    Methyltransferase-like 3 (METTL3) plays a crucial role in post-transcriptional gene regulation. Substantial evidence links METTL3 to various immune dysfunctions, such as the suppression of antiviral immunity during viral infections and the disruption of immune tolerance in conditions like autoimmune diseases, myeloid leukemia, skin cancers, and anticancer immunotherapy. However, a thorough review and analysis of this evidence is currently missing, which limits the understanding of METTL3's mechanisms and significance in immune dysfunctions. This review aims to elucidate the roles and mechanisms of METTL3 in these immune issues, highlighting its connections and proposing new insights into its modulation of immune responses. Analysis results in this review suggest that METTL3 hampers antiviral immunity, worsens viral replication and infection, and disrupts immune tolerance; conversely, regulating METTL3 enhances antiviral immunity and facilitates viral clearance. Moreover, clinical data corroborates these findings, showing that METTL3 overexpression is associated with increased susceptibility to viral infections and autoimmune conditions. This review establishes a theoretical basis for considering METTL3 as a novel regulator, an important diagnostic biomarker, and a potential target for treating immune dysfunctions.

    Keywords: methyltransferase-like 3, immune dysfunction, antiviral immunity, Immune Tolerance, Diagnostic biomarker, Therapeutic target

    Received: 07 Nov 2024; Accepted: 11 Mar 2025.

    Copyright: © 2025 Zhang, Xu, Gao, Qu and Su. 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: Xiaojuan Su, West China Second University Hospital, Sichuan University, Chengdu, China

    Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.

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