Fig. 9: Epigenetic reprogramming of trained TLR4+ILC2 in the mouse type 2 inflammatory model.
From: TLR4+group 2 innate lymphoid cells contribute to persistent type 2 immunity in airway diseases

A Schematic diagram of the experimental study design for scATAC-seq of lung tissues from wide-type HDM sensitized mice. B Uniform manifold approximation and projection (UMAP) plots of sorted viable CD45+Lin⁻ICOS+ST2+cells from HDM-sensitized mice at day 45 and day 47. Each dot represents a single cell, with different ILC2 subsets shown in different colors. C Alteration of chromatin accessibility in the ILC2_c02 subset at day 47 versus day 45. The Y axis presents the log2 fold change of gene activity at day 47 versus day 45 and in library 2, while the X axis shows the log2 fold change in library 1. D Transcription factor binding motifs significantly enriched in the ILC2_c02 subset at day 47 versus day 45. P-values were calculated by a right-tailed hypergeometric test. E DNA accessibility tracing of the Tlr4 and Il1rl1 of different ILC2 subsets. Shaded boxes delineate increased chromatin accessibility. F Predicted motifs within Tlr4 promoter. G Motif footprinting trace showing binding activities of transcription factor JunB, Fos, PU.1 and MafK.