Molecular Characterization of Murine Defa6-Expressing Paneth Cells

Paneth Cell abnormalities have been implicated in several human gastrointestinal diseases, but the precise mechanisms by which PC dysfunction contributes to disease pathogenesis remains unclear. This is due in part to limited approaches to isolate viable PCs for downstream analysis. Previously reported methods include sorting for PCs using CD24-based strategies, or via promotor activation of PC-specific genes such as Defa4, Lyz1, or Defa24. Collectively, these studies have demonstrated greater than expected heterogeneity of the PC population. In the present study, we further characterize this heterogeneity using a Defa6iCre; Rosa26LSL-tdTomato (Defa6Tom) reporter model.