期刊
CELL
卷 166, 期 5, 页码 1231-+出版社
CELL PRESS
DOI: 10.1016/j.cell.2016.07.043
关键词
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资金
- Boehringer Ingelheim Fonds PhD Fellowship
- Abisch Frenkel Foundation for the Promotion of Life Sciences
- Gurwin Family Fund for Scientific Research
- Leona M. and Harry B. Helmsley Charitable Trust
- Crown Endowment Fund for Immunological Research
- estate of J. Gitlitz
- estate of L. Hershkovich
- Benoziyo Endowment Fund for the Advancement of Science
- Adelis Foundation
- French National Center for Scientific Research (CNRS)
- European Research Council
- Marie Curie Integration grant
- German-Israeli Foundation for Scientific Research and Development
- Israel Science Foundation
- Minerva Foundation
- Rising Tide Foundation
- Helmholtz Foundation
- European Foundation for the Study of Diabetes
- European Research Council [309788]
- Israel Science foundation [782/11]
- BLUEPRINT FP7 consortium
- Ernest and Bonnie Beutler Research Program of Excellence in Genomic Medicine
- Minerva Stiftung research grant
- National Human Genome Research Institute Center for Excellence in Genome Science [1P50HG006193]
- Israeli Ministry of Science, Technology and Space
- David and Fela Shapell Family Foundation
- Abramson Family Center for Young Scientists
- European Research Council (ERC) [309788] Funding Source: European Research Council (ERC)
Innate lymphoid cells (ILCs) are critical modulators of mucosal immunity, inflammation, and tissue homeostasis, but their full spectrum of cellular states and regulatory landscapes remains elusive. Here, we combine genome-wide RNA-seq, ChIP-seq, and ATAC-seq to compare the transcriptional and epigenetic identity of small intestinal ILCs, identifying thousands of distinct gene profiles and regulatory elements. Single-cell RNA-seq and flow and mass cytometry analyses reveal compartmentalization of cytokine expression and metabolic activity within the three classical ILC subtypes and highlight transcriptional states beyond the current canonical classification. In addition, using antibiotic intervention and germ-free mice, we characterize the effect of the microbiome on the ILC regulatory landscape and determine the response of ILCs to microbial colonization at the single-cell level. Together, our work characterizes the spectrum of transcriptional identities of small intestinal ILCs and describes how ILCs differentially integrate signals from the microbial microenvironment to generate phenotypic and functional plasticity.
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