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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE273588 | GEO | 2024/10/09

REPOSITORIES: GEO

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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]

2024-10-09 | GSE273584 | GEO

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

2024-10-09 | GSE273585 | GEO

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

2024-10-09 | GSE273587 | GEO

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

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

| PRJNA1142465 | ENA

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]

| PRJNA1142467 | ENA

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]

| PRJNA1142468 | ENA

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]

| PRJNA1142469 | ENA

IgA EGFR antibodies mediate tumour killing in vivo.

Project description:Currently all approved anti-cancer therapeutic monoclonal antibodies (mAbs) are of the IgG isotype, which rely on Fcgamma receptors (Fc?Rs) to recruit cellular effector functions. In vitro studies showed that targeting of Fc?RI (CD89) by bispecific antibodies (bsAbs) or recombinant IgA resulted in more effective elimination of tumour cells by myeloid effector cells than targeting of Fc?R. Here we studied the in vivo anti-tumour activity of IgA EGFR antibodies generated using the variable sequences of the chimeric EGFR antibody cetuximab. Using Fc?RI transgenic mice, we demonstrated significant in vivo anti-tumour activity of IgA2 EGFR against A431 cells in peritoneal and lung xenograft models, as well as against B16F10-EGFR cells in a lung metastasis model in immunocompetent mice. IgA2 EGFR was more effective than cetuximab in a short-term syngeneic peritoneal model using EGFR-transfected Ba/F3 target cells. The in vivo cytotoxic activity of IgA2 EGFR was mediated by macrophages and was significantly decreased in the absence of Fc?RI. These results support the potential of targeting Fc?RI for effective antibody therapy of cancer.

| S-EPMC3944462 | biostudies-literature

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