Chromatin assembly factor 1B critically controls the early development but not function acquisition of invariant natural killer T cells in mice

CD4+CD8+ double-positive thymocytes give rise to both conventional TCRαβ+ T cells and invariant natural killer (iNKT cells), but these two kinds of display different characteristics. The molecular mechanism underlying iNKT cell lineage development function acquisition remain be elucidated. We show that the loss chromatin assembly factor 1B (CHAF1b) maintains normal severely impairs early cells. This dysregulation is accompanied by impairment in activation gene transcription at Vα14-Jα18 locus. Notably, ectopic expression a TCR rescues Chaf1b-deficient developmental defects. Moreover, cytokine secretion antitumor activity are substantially maintained transgene-rescued Our study identifies CHAF1b as critical controls not via lineage- stage-specific regulation.