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ITPK1 sensitizes tumor cells to IgA-dependent neutrophil killing in vivo

ABSTRACT: ITPK1 sensitizes tumor cells to IgA-dependent neutrophil killing in vivo

PROVIDER: PRJNA1142465 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30051506.fastq.gz	Fastqsanger.gz
	SRR30051507.fastq.gz	Fastqsanger.gz
	SRR30051528.fastq.gz	Fastqsanger.gz
	SRR30051529.fastq.gz	Fastqsanger.gz
	SRR30051530.fastq.gz	Fastqsanger.gz

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ITPK1 sensitizes tumor cells to IgA-dependent neutrophil killing in vivo [CRISPR focused]

Project description:Neutrophils can efficiently trigger cytotoxicity towards tumor cells and other target cells upon engagement of the IgA receptor CD89. However, the cell-intrinsic factors that influence the induction of cell death upon exposure to neutrophil effector mechanisms in vivo remain largely unknown. To uncover genetic regulators that influence target cell sensitivity to IgA-induced neutrophil-mediated killing, we used a human CD89 (hCD89) transgenic mouse model in which IgA-mediated killing of Her2-positive CD47-deficient murine target cells is mediated by neutrophils. Using a genome-wide in vivo screening approach, we demonstrate that deletion of the gene encoding inositol-tetrakisphosphate 1 kinase, ITPK1, increases survival of target cells in anti-Her2 IgA-treated mice. Moreover, we show that this effect depends on neutrophil activity and on the ITPK1 kinase domain. Notably, ITPK1 deficiency did not measurably impact survival of IgA-opsonized target cells in in vitro systems, underscoring the importance of in vivo screening systems to uncover physiologically relevant regulators of neutrophil killing.

2024-10-09 | GSE273586 | GEO

ITPK1 sensitizes tumor cells to IgA-dependent neutrophil killing in vivo [RNA-seq]

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ITPK1 sensitizes tumor cells to IgA-dependent neutrophil killing in vivo [CRISPR Epistasis]

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ITPK1 sensitizes tumor cells to IgA-dependent neutrophil killing in vivo [CRISPR genome-wide]

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ITPK1 sensitizes tumor cells to IgA-dependent neutrophil killing in vivo [CRISPR Epistasis]

Project description:ITPK1 sensitizes tumor cells to IgA-dependent neutrophil killing in vivo [CRISPR Epistasis]

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ITPK1 sensitizes tumor cells to IgA-dependent neutrophil killing in vivo [RNA-seq]

Project description:ITPK1 sensitizes tumor cells to IgA-dependent neutrophil killing in vivo [RNA-seq]

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ITPK1 sensitizes tumor cells to IgA-dependent neutrophil killing in vivo [CRISPR focused]

Project description:ITPK1 sensitizes tumor cells to IgA-dependent neutrophil killing in vivo [CRISPR focused]

| PRJNA1142470 | ENA

ITPK1 sensitizes tumor cells to IgA-dependent neutrophil killing in vivo [CRISPR genome-wide]

Project description:ITPK1 sensitizes tumor cells to IgA-dependent neutrophil killing in vivo [CRISPR genome-wide]

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ITPK1 sensitizes tumor cells to IgA-dependent neutrophil killing in vivo

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-10-09 | GSE273588 | GEO

Neutrophil extracellular traps melt Peyer’s patches following stroke and myocardial infarction

Project description:Sterile tissue injury after stroke causes lymphocyte contraction in lymphoid tissues and may decrease circulating IgA-levels. Intestinal Peyer’s patches (PP) harbor large numbers of IgA+ B cell precursors and plasma cells. Whether and how tissue injury triggers PP-B cell death, thereby mediating IgA-loss, is unknown. We found decreased circulating IgA levels in stroke and myocardial infarction patients. Experimental stroke and myocardial infarction in mice phenocopied the human situation. Decreased plasma and fecal IgA were accompanied by rapid and macroscopic shrinkage of PP caused by substantial losses of PP-resident IgA+ precursors and plasma cells in mice. Tissue injury induced neutrophil activation endowed with the release of toxic neutrophil extracellular traps (NETs). Antibody-mediated or genetically- induced neutrophil loss, digestion of NETs, or inhibition of their release by the Gasdermin D blockade completely prevented lymphocyte loss and PP shrinkage. We also identified NETs in the plasma of stroke and myocardial infarction patients. Hence, tissue injury induces systemic NET-release, which might be targeted to maintain immune homeostasis at mucosal barriers.

2024-02-28 | PXD044644 | Pride

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