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Menin orchestrates macrophage reprogramming to maintain the pulmonary immune homeostasis

GSE240958 Mus musculus Genome binding/occupancy profiling by high throughput sequencing 28 samples 2024/12/25 GPL17021
Summary
The potential importance of menin in immune regulation remains unclear. Here, we report that myeloid deletion of Men1 results in the development of spontaneous pulmonary alveolar proteinosis (PAP). This is strongly correlated with impaired development of alveolar macrophages (AM) and epigenetic inactivation of the GM-CSF pathway caused by Men1 deficiency. Mechanistically, menin directly interacts with SETD2 and collectively maintain GM-CSF expression through H3K36me3, which orchestrates AM reprogramming and pulmonary immune homeostasis.
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