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This review analyzes how m6A modification affects immune cell function in Th2-driven allergic responses, suggesting therapeutic avenues.
Th2-driven allergic responses are characterized by allergic reactions and immune dysregulation with complex pathogenesis that warrants urgent in-depth study. The predominant posttranscriptional modification observed in eukaryotic messenger RNAs, N6-methyladenosine (m6A), dynamically regulates RNA splicing, which is likely regulated during cell fate determination, cytokine production, and epithelial barrier maintenance in context of Th2-driven allergic responses. This review systematically analyzes the effects of m6A modification on the differentiation and functional regulation of major immune cell populations, including dendritic cells, macrophages, T helper cells, B cells, and mast cells, as well as barrier-forming epithelial cells. Additionally, we discuss how m6A regulators control the transcription of cytokine-encoding genes, transcription factors that regulate T-cell function, and T lymphocyte activation signals. Furthermore, this paper integrates the latest research advancements and explores the application potential of m6A modification for diagnosis and treatment of Th2-driven allergic disorders, including allergic asthma and rhinitis. By presenting a summary of the current progress in this area of research, this paper aims at summarizing the role of m6A modification during Th2-driven allergic responses and highlight its therapeutic potential and future research directions.
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Wang et al. (2026) studied this question.
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