ArticleCell communication and signaling : CCS2024
Dust mite antigens endow dendritic cells with the capacity to induce a Th2 response by regulating their methylation profiles.
Article in Cell communication and signaling : CCS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed.
- Article
- The human 18S rRNA m6A methyltransferase METTL5 promotes tumorigenesis via DEPDC1 in lung squamous cell carcinoma.Frontiers in oncology · 2025Article
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13 authors.
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Abstract
backgroundIt is well-known that Dendritic cells (DCs) are essential in the development of airway Th2 polarization and airway allergy (AA). The underlying mechanism is still not fully understood. The objective of this study is to examine the role of methyltransferase-like protein-5 (Mettl5), a methyltransferase involved in N6-methyladenosine (m6A) methylation, in altering DC's properties to facilitate the development of Th2 polarization and AA.
methodsDust mite extracts (DME) were used as a specific antigen to establish an AA mouse model. The epigenetic status of DCs was examined using a Chromatin immunoprecipitation (ChIP) assay. A mouse strain carrying the Mettl5-deficient DCs was used to observe the role of Mettl5 in determining the phenotypes of DCs.
resultsThe results showed that the expression of Mettl5 was elevated in DCs, which was positively correlated with the AA response. The development of airway Th2 polarization was hindered by Mettl5 depletion in DCs. Mettl5 is involved in the transcription of the Timd4 gene in DCs caused by DME. The degradation of IRF5 by Mettl5 led to an increase in T cell immunoglobulin domain molecule-4 (TIM4) expression in DCs associated with DME. Inhibition of Mettl5 in DCs reconciled the DME-induced airway Th2 polarization and experimental AA.
conclusionsAirway DCs from AA mice showed elevated amounts of Mettl5, which led to the expression of TIM4. The experimental AA was mitigated by Mettl5 inhibition.
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