In vivo G-CSF Treatment Activates GR-SOCS1 Axis Suppressing IFN-? Secretion by Natural Killer Cells

By comparing the multi-omics profile of human NK cells before and after G-CSF in vivo treatment, we identified a pathway that was activated in response to G-CSF treatment, which suppressed IFN-? secretion in NK cells. Specifically, integrative genomic strategy uncovered that glucocorticoid receptor (GR) was activated and mediated the genomic response to G-CSF treatment in NK cells. Activated GR can inhibit secretion of IFN-? via promoting interactions between suppressor of cytokine signaling 1 (SOCS1) promoter and enhancer and increase the expression of SOCS1. Overall design: We performed GR CUT&Tag in NK92 cells to aquire whole genome GR bingding information. Also, H3K27ac CUT&Tag was performed to identify enhancer regions in NK92 cells. Please note that each processed data was generated from both replicates and is linked to the corresponding rep1 sample records.