cell influx post irradiation or colitis. By contrast, depleting tetrameric STAT5 in organoids reduced ISC pluripotency and organoid growth post irradiation. Mechanistically, chromatin immunoprecipitation and single-cell RNA sequencing analyses with crypt cells revealed that depleting STAT5 tetramers decreased STAT5-binding on the Metallothionein 1 (Mt1) locus in crypt T cells and increased Mt1 expression, which leads to T cell migration into crypts and enhanced ISC regeneration. Together, the tetrameric STAT5 suppresses the formation of the crypt T cell niche. Interrupting STAT5 tetramers promotes the expansion of crypt TCRγδ cells, providing a target for promoting ISC regenerative repair during IBD-ulcerative colitis.
Li et al. (Fri,) studied this question.