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The AP-1/JNK pathway is regulated by CD73 and gets dysregulated in aged hosts leading to defect in anti-pneumococcal function of neutrophils

ABSTRACT: The AP-1/JNK pathway is regulated by CD73 and gets dysregulated in aged hosts leading to defect in anti-pneumococcal function of neutrophils

PROVIDER: PRJNA633715 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11809830_1.fastq.gz	Fastqsanger.gz
	SRR11809830_2.fastq.gz	Fastqsanger.gz
	SRR11809831_1.fastq.gz	Fastqsanger.gz
	SRR11809831_2.fastq.gz	Fastqsanger.gz
	SRR11809832_1.fastq.gz	Fastqsanger.gz

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The AP-1/JNK pathway is regulated by CD73 and gets dysregulated in aged hosts leading to defect in anti-pneumococcal function of neutrophils

Project description:We used high through put RNA-sequencing to identify changes in the PMN transcriptome induced by S. pneumoniae infection in order to gain further insight into the signaling pathways that are required for host response and are dysregulated in older individuals. PMNs were isolated from bone marrow of young WT, old WT and CD73KO mice and challenged with S.pneumonia TIGR4 strain in-vitro. Analysis of differentially expressed genes revealed that genes in AP-1/JNK pathway were upregulated in PMNs from CD73KO and old mice but not in PMNs from young mice. Inhibition of AP-1 and JNK using inhibitors boosted the anti-microbial actiivity of neutrophils from old and CD73KO mice.

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Project description:High levels of ecto-5'-nucleotidase (CD73) have been implicated in immune suppression and tumor progression. Elevated levels of CD73 has also been observed in patients who progress on anti–PD-1 immunotherapy. While regulatory T cells can express CD73 and inhibit T cell responses via the production of adenosine, less is known if conventional T cells and natural killer (NK) cells can express CD73. We found that the expression of CD73 is restricted to tumor-infiltrating NK cells and the frequency of these cells correlate with larger tumor size in patients with breast cancer. In addition, the expression of other immune checkpoint receptors including LAG-3 and VISTA was significantly higher in CD73 positive NK cells than on CD73 negative NK cells. Furthermore, the prognostic value of CD73 gene expression was influenced by NK cell signature expressed in patients with breast cancer and sarcoma. Mechanistically, upon engagement of 4-1BBL on tumor cells, NK cells transport CD73 in intracellular vesicles to the cell surface and extracellular space via actin polymerization-dependent exocytosis. These CD73 positive NK cells undergo transcriptional reprogramming and upregulate IL10 production via STAT3 transcriptional activity and suppress CD4 T cell activity. Altogether, our results support that tumors can hijack NK cells as a means to escape immunity and that CD73 expression defines an inducible population of NK cells with immune regulatory properties within the tumor microenvironment.

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