Host-microbial crosstalk relies on “tuft” love

How commensals influence intestinal immunity is incompletely understood. In this issue of Immunity, Eshleman et al. demonstrate that microbiota-derived butyrate restrains tuft cell development via HDAC3 modulation in intestinal epithelial cells, showing how microbial metabolites impact intestinal type 2 immunity. How commensals influence intestinal immunity is incompletely understood. In this issue of Immunity, Eshleman et al. demonstrate that microbiota-derived butyrate restrains tuft cell development via HDAC3 modulation in intestinal epithelial cells, showing how microbial metabolites impact intestinal type 2 immunity. Microbiota-derived butyrate restricts tuft cell differentiation via histone deacetylase 3 to modulate intestinal type 2 immunityEshleman et al.ImmunityJanuary 30, 2024In BriefTuft cells are central regulators of type 2 immunity in the intestine. Eshleman et al. reveal that commensal bacterial-derived butyrate restricts stem cell development into tuft cells through the epigenetic-modifying enzyme HDAC3. The microbiota can therefore direct tuft cell numbers in the intestine to fine-tune mucosal immunity. Full-Text PDF