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A novel model of pulmonary KPC infection reveals critical roles of NK cell and group 3 ILC cytokines in host resistance

ABSTRACT: A novel model of pulmonary KPC infection reveals critical roles of NK cell and group 3 ILC cytokines in host resistance

PROVIDER: PRJNA533635 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8929010.fastq.gz	Fastqsanger.gz
	SRR8929011.fastq.gz	Fastqsanger.gz
	SRR8929012.fastq.gz	Fastqsanger.gz
	SRR8929013.fastq.gz	Fastqsanger.gz
	SRR8929014.fastq.gz	Fastqsanger.gz

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A novel model of pulmonary KPC infection reveals critical roles of NK cell and group 3 ILC cytokines in host resistance

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Project description:Innate lymphoid cells (ILCs) represent innate versions of T helper and cytotoxic T cells that differentiate from committed ILC precursors (ILCP). Still, how ILCP relate to mature tissue-resident ILCs remains unclear. We identify ILCP that are present in the blood and all tested lymphoid and non-lymphoid human tissues. Human ILCP fail to express the signature transcription factors (TF) and cytokine outputs of mature NK cells and ILCs but are epigenetically poised to do so. Human ILCP robustly generate all ILC subsets in vitro and in vivo. While human ILCP express RAR related orphan receptor C (RORC), circulating ILCP can be found in RORC-deficient patients that retain potential for EOMES+ NK cells, T-BET+ ILC1, GATA-3+ ILC2 and for IL-22+ but not for IL-17A+ ILC3. We propose a model of tissue ILC differentiation (‘ILC-poiesis’) whereby diverse ILC subsets are generated in situ from ILCP in response to environmental stressors, inflammation and infection.

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