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ID2 is required for binding of BATF/AP-1-related family transcription factors to genes associated with NK cell effector maturation Barbara L. Kee, Yiying Xu, Erin C. Zook, Renee dePooter, and Zhong-Yin Li. Dept. of Pathology and Committee on Immunology, University of Chicago, Chicago IL USA, 60615. Id2 is an inhibitor of the E protein transcription factors that is required for the development of mature NK cells. Here we show that mature NK cells develop in the absence of Id2 but fail to progress from the naïve KLRG1-CD27+CD11b- stage to the effector KLRG1+CD27-CD11b+ stage. The cytotoxic effector program that characterizes this transition, including transcription of Gzmb Il18r1, Il1rl1, Ifng and Prf1, is not initiated in the absence of Id2. Instead, Id2-deficient naïve NK cells up-regulate expression of multiple T lymphocyte associated transcripts encoding cytokine and chemokine receptors as well as intracellular signaling proteins. A transposase accessible chromatin (ATAC)-seq analysis revealed an increase in open chromatin at E protein binding sites in upregulated genes confirming heightened E protein activity. In contrast, in the absence of Id2 there was a loss of open chromatin at NK cell effector genes that was associated with sequences bound by signal regulated transcription factors of the BATF/AP-1 family. Our data reveal a possible role for BATF/AP-1 transcription factors in naïve NK cells to promote the expression of the cytotoxic effector program of mature NK cells. Sessions: NK cell development and differentiation, Innate lymphoid cells.