TY - JOUR
T1 - Tissue signals imprint ILC2 identity with anticipatory function
AU - Ricardo-Gonzalez, Roberto R.
AU - Van Dyken, Steven J.
AU - Schneider, Christoph
AU - Lee, Jinwoo
AU - Nussbaum, Jesse C.
AU - Liang, Hong Erh
AU - Vaka, Dedeepya
AU - Eckalbar, Walter L.
AU - Molofsky, Ari B.
AU - Erle, David J.
AU - Locksley, Richard M.
N1 - Publisher Copyright:
© 2018, The Author(s), under exclusive licence to Springer Nature America, Inc.
PY - 2018/10/1
Y1 - 2018/10/1
N2 - Group 2 innate lymphoid cells (ILC2s) are distributed systemically and produce type 2 cytokines in response to a variety of stimuli, including the epithelial cytokines interleukin (IL)-25, IL-33, and thymic stromal lymphopoietin (TSLP). Transcriptional profiling of ILC2s from different tissues, however, grouped ILC2s according to their tissue of origin, even in the setting of combined IL-25-, IL-33-receptor-, and TSLP-receptor-deficiency. Single-cell profiling confirmed a tissue-organizing transcriptome and identified ILC2 subsets expressing distinct activating receptors, including the major subset of skin ILC2s, which were activated preferentially by IL-18. Tissue ILC2 subsets were unaltered in number and expression in germ-free mice, suggesting that endogenous, tissue-derived signals drive the maturation of ILC2 subsets by controlling expression of distinct patterns of activating receptors, thus anticipating tissue-specific perturbations occurring later in life.
AB - Group 2 innate lymphoid cells (ILC2s) are distributed systemically and produce type 2 cytokines in response to a variety of stimuli, including the epithelial cytokines interleukin (IL)-25, IL-33, and thymic stromal lymphopoietin (TSLP). Transcriptional profiling of ILC2s from different tissues, however, grouped ILC2s according to their tissue of origin, even in the setting of combined IL-25-, IL-33-receptor-, and TSLP-receptor-deficiency. Single-cell profiling confirmed a tissue-organizing transcriptome and identified ILC2 subsets expressing distinct activating receptors, including the major subset of skin ILC2s, which were activated preferentially by IL-18. Tissue ILC2 subsets were unaltered in number and expression in germ-free mice, suggesting that endogenous, tissue-derived signals drive the maturation of ILC2 subsets by controlling expression of distinct patterns of activating receptors, thus anticipating tissue-specific perturbations occurring later in life.
UR - http://www.scopus.com/inward/record.url?scp=85053319624&partnerID=8YFLogxK
U2 - 10.1038/s41590-018-0201-4
DO - 10.1038/s41590-018-0201-4
M3 - Article
C2 - 30201992
AN - SCOPUS:85053319624
SN - 1529-2908
VL - 19
SP - 1093
EP - 1099
JO - Nature immunology
JF - Nature immunology
IS - 10
ER -