| First Author | Ricardo-Gonzalez RR | Year | 2018 |
| Journal | Nat Immunol | Volume | 19 |
| Issue | 10 | Pages | 1093-1099 |
| PubMed ID | 30201992 | Mgi Jnum | J:282645 |
| Mgi Id | MGI:6381278 | Doi | 10.1038/s41590-018-0201-4 |
| Citation | Ricardo-Gonzalez RR, et al. (2018) Tissue signals imprint ILC2 identity with anticipatory function. Nat Immunol 19(10):1093-1099 |
| abstractText | 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. |
