N6-methyladenosine (m6A) serves as a critical RNA modification, dynamically governing RNA metabolism through its influence on RNA stability, splicing, translation, and degradation. In recent years, m6A has emerged as a critical regulator orchestrating the development, differentiation, and other functions of immune cells. Immune cells are the front-line defenders against pathogens. Abnormal activation or dysfunction of these cells can result in chronic inflammation, tissue damage, and a variety of diseases, including rheumatoid arthritis (RA), atherosclerosis, non-alcoholic fatty liver disease, and cancer. Research has shown that m6A modification regulates immune cell polarization, cytokine production, and metabolic reprogramming. For instance, m6A methylation mediated by METTL3 stabilizes transcription factor mRNAs (e.g., STAT1), which promotes the differentiation of macrophages towards the pro-inflammatory M1 phenotype. Conversely, FTO-dependent demethylation suppresses SOCS1 expression, intensifies the TLR4/NF-κB signaling pathway, and boosts the secretion of pro-inflammatory cytokines like IL-6 and TNF-α. Moreover, m6A modification also has an impact on immune cell metabolism by modulating key metabolic regulators (such as HIF-1α and PPARγ). In diseases like RA and atherosclerosis, the dysregulation of m6A in macrophages exacerbates the release of inflammatory cytokines and the formation of plaques. In tumors, tumor-associated macrophages with altered m6A modification contribute to the establishment of an immunosuppressive microenvironment. Meanwhile, the dysfunction of natural killer cells due to METTL3 deficiency undermines antitumor immunity. Collectively, these findings position m6A as an epigenetic regulator of immune cell function, which holds profound implications for inflammatory diseases.

This Research Topic aims to provide insights into the role of m6A modification in immune cell-regulated inflammatory diseases and to explore the detailed molecular mechanisms by which m6A modulates immune cell functions, such as polarization, cytokine production, and metabolic reprogramming in various inflammatory diseases. Additionally, we seek to identify novel therapeutic targets and strategies based on the understanding of m6A-mediated immune cell regulation.

To this end, we encourage submission of Original Research articles, Perspectives, Clinical Trials, Reviews, Mini-Reviews covering, but not limited to, the following subtopics:

1) The role of m6A writers, readers, and erasers in modulating immune cell-mediated inflammation;
2) The role of m6A modification on immune cell development, differentiation, activation, and effector functions;
3) The crosstalk between m6A modification and other epigenetic mechanisms, such as DNA methylation and histone modification, in immune cell regulation;
4) The impact of m6A modification on immune cell metabolism and its relationship with inflammatory diseases;
5) The development and application of novel technologies for studying m6A modification in immune cells;
6) Potential therapeutic strategies targeting m6A modification in inflammatory diseases

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m6A modification in immune cell-regulated inflammatory diseases