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Article Abstract
Group 2 innate lymphoid cells (ILC2s) represent one of the major drivers of allergic inflammation; however, the precise mechanisms governing the development and function of ILC2s remain unknown. Here, we show that the transcription factor BACH2 was abundantly expressed and epigenetically activated in ILC2s and their progenitors. Conditional ablation of BACH2 diminished the ability of ILC2 progenitors to differentiate into ILC2s. Integration of the scRNA-seq, ATAC-seq, and CUT&Tag-seq techniques revealed that BACH2 modulated the transcriptional profiles and epigenetic landscapes of ILC2 progenitors. Furthermore, BACH2 ablation compromised the functionality of ILC2s, resulting in a resolution of allergic airway inflammation. Notably, the different binding sites of BACH2 in ILC2s and T2 cells suggested that BACH2 binds to IRF4 to control the function of ILC2, underscoring its context-specific effects on allergic airway inflammation. These findings shed promising light on the importance of BACH2 in type 2 immunity and its multifaceted role in asthma.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC12315961 | PMC |
| http://dx.doi.org/10.1126/sciadv.ads4323 | DOI Listing |
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