Extended Data Fig. 7: Skin ILC similarities to and differences from mouse bone marrow and lung ILC precursors.
From: Skin-resident innate lymphoid cells converge on a pathogenic effector state
a, ILC-precursor markers have distinctive expression patterns in skin ILCs. Although IL-18Rα+ST2– ILC2s were identified as precursors in lung17,18, most skin ILCs express Il18r1 but not Il1rl1 (as in Fig. 1i), and Klf2 is highest in quiescent-like cells (as in Fig. 1g). FDL embedding (as in Fig. 1e) shows cell profiles (dots) from all time points, coloured by normalized expression (log-transformed scTransform-corrected counts, Methods; colour bar; low, grey; high, maroon) of precursor-associated genes, including those that are broadly expressed in skin ILCs (top row, Il18r1, Tcf7, Tox and Itgb7), highly expressed in topic-2-high (‘ILC2’) cells (middle row, Itga4 and Kit), lowly expressed in topic-1-high (‘quiescent-like’) cells (middle row, negative marker Il2ra, which encodes CD25), or highly expressed in topic-3-high (‘ILC3-like’) cells (bottom row, Zbtb16, Pdcd1, Tox2, Selenop and Gimap5). Note that integrin proteins encoded by Itgb7 and Itga4 form the heterodimeric integrin receptor α4β7. b, Klf2 expression is associated with high Il18r1 and low Il1rl1 expression in lung ILCs35, both in steady state and in induced ‘inflammatory ILC2s’7. t-distributed stochastic neighbour embedding (tSNE) of lung-resident ILCs (dots), coloured by experimental condition (top row: PBS control, dark grey; orange, IL-25 stimulation; blue, IL-33 stimulation; light grey, cells from other conditions), and by logTPX (Methods) normalized expression (bottom row: colour bar: low, grey; high, red) of genes used to delineate lung precursors17 (Il18r1 and Il1rl1), ‘quiescent-like’ topic 1-associated Klf2, ILC3-required transcription factor Rorc, and IL-25-induced ‘inflammatory-ILC2’ marker Klrg1.
