c-Maf regulates the plasticity of group 3 innate lymphoid cells by restraining the type 1 program [ATAC-seq]

The transcription factor c-Maf is an essential regulator of group 3 ILC homeostasis and effector plasticity. c-Maf limits acquisition of the type 1 program and conversion to the ILC1 fate through restraint of T-bet expression and function. Overall design: Evaluation of differential ATAC-seq accessibilty in cohoused Maf-deficient NKp46+ ILC3 and CCR6+ ILC3. The Omni ATAC protocol was performed on replicate samples of both NKp46+ ILC3 and CCR6+ ILC3s isolated from the small intestine lamina propria of Maf+/+ Il7r-Cre and Maf fl/fl Il7r-Cre mice. Evaluation of ATAC-seq accessibilty during transition of DN ILC3 to NKp46+ ILC3 to ILC1 using both C57Bl/6 and Rorc(t) GFP/+ mice. The Omni ATAC protocol was performed on replicate samples for each population isolated from the small intestine lamina propria of C57Bl/6 and Rorc(t) GFP/+ mice.