The transcriptional repressor HIC1 is required for the maintenance of tissue-resident ILC1

Abstract The group 1 innate lymphoid cell compartment is comprised of conventional natural killer (cNK) and type cells (ILC1). Within the pool, these are delineated by expression transcription factor TBET, both subtypes express surface receptors NK1.1 NKp46. Functionally, ILC1 cNK have been shown to mediate pathogen clearance tumour control through release cytokines, particularly IFN-□. While being closely related, a key feature distinguishing from their propensity reside within tissue niche rather than enter circulation. However, precise mechanisms that regulate residency ILC1s remain unknown. Here, we show Hypermethylated in Cancer (HIC1) critical point development maintenance ILC1. In liver, HIC1 restricted compartment. Deletion NKp46 +cells (Hic1 ΔNcr1mice) resulted specific significant reduction liver-resident ILC1, while were unaffected. Additionally, isolated Hic1 ΔNcr1mice incapable restoring lymphocyte-deficient hosts, unlike wild donors. Thus, our results identify an important role for peripheral