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RNA expression NKp44- ILC3s and NKp44+ ILC3s in lung cancer

ABSTRACT: RNA expression NKp44- ILC3s and NKp44+ ILC3s in lung cancer

PROVIDER: PRJNA554782 | ENA |

REPOSITORIES: ENA

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RNA expression NKp44- ILC3s and NKp44+ ILC3s in lung cancer

Project description:Purpose: To detect RNA-seq of NKp44- ILC3s and NKp44+ ILC3s in lung cancer and find the differences between these tow group. Results:Compared with those of NKp44+ILC3s, NKp44-ILC3s had 12,965 DEGs, with 6161 up-regulated genes and 6804 down-regulated genes,most DEGs related to the functions of cellular process, biological regulation, cell component, and molecular binding.

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Project description:Group 3 innate lymphoid cells (ILC3s) are abundant in the developing or healthy intestine to critically support tissue homeostasis in response to microbial cues and other environmental signals. However, during gastrointestinal disease including infections, colorectal cancer, or inflammatory bowel disease (IBD), intestinal ILC3 numbers are dramatically reduced and the remaining ILC3s become dysfunctional which fuels disease and barrier breakdown. To define the underlying transcriptomic changes, we employed RNA sequencing of ILC3s from IBD patients. This may help to gain a deeper understanding of the mechanisms driving these alterations and ultimately lead to novel preventive, diagnostic, or therapeutic opportunities in IBD.

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Project description:ILC3s from the spleen (SP) and small intestine (SI) have been shown to be phenotypically and functional different. Intestinal factors are likely to regulate transcriptional profiles and thereby function of ILC3s. The goal of this study is to analyze if SI ILC3s acquire a SP-similar transcriptional profile after in vitro culture. Therefore transcriptional profiles of cultured SI ILC3s were compared to freshly isolated ILC3s of the murine SP and the SI by RNA seq technology. Cell suspension were generated from both organs and ILC3s (CD117+, Thy1.2+, KLRG1-, lin- (CD3, CD8, CD11b, CD11c, CD19, B220, Gr-1, TCRβ, TCRγδ, TER-119, NK1.1)) were sort purified. SI ILC3 were cultured for 7 days in vitro with IL-2, IL-7 and SCF. RNA was isolated and RNA sequencing was done using Ilumina Hiseq 2500 system and NuGEN Ovation RNA Seq System V2, with biological replicates. We show that intestinal ILC3 acquire a splenic-similar transcriptional profile after in vitro culture.

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Project description:Group 3 innate lymphoid cells (ILC3s) are critical regulators of intestinal homeostasis, yet their role in cancer remains elusive. Here, we identify that the tumor microenvironment of humans and mice with colorectal cancer (CRC) contains altered ILC3 responses that resemble those found during intestinal inflammation and are characterized by reduced frequencies, altered subset distribution, and an imbalance with T cells. We evaluated the consequences of these changes in mice and determined that ILC3-specific major histocompatibility complex class II (MHCII) was required to limit the progression of CRC. Interestingly, ILC3-specific MHCII also prevented resistance to anti-PD-1 immunotherapy by regulating intestinal inflammation and microbiota composition. Finally, humans with intestinal inflammation and dysregulated ILC3s also harbor specific microbiota that are sufficient to promote immunotherapy resistance in mice. Collectively, these data define a protective role for antigen-presenting ILC3s in cancer, and indicate that inherent disruption of this pathway drives CRC progression and immunotherapy resistance.

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2020-03-17 | GSE114749 | GEO

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