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CALHM6 is an immunological synapse ion channel required for macrophage-natural killer cell communication upon bacterial infection

ABSTRACT: CALHM6 is an immunological synapse ion channel required for macrophage-natural killer cell communication upon bacterial infection

PROVIDER: PRJNA924701 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23097418_1.fastq.gz	Fastqsanger.gz
	SRR23097418_2.fastq.gz	Fastqsanger.gz
	SRR23097419_1.fastq.gz	Fastqsanger.gz
	SRR23097419_2.fastq.gz	Fastqsanger.gz
	SRR23097420_1.fastq.gz	Fastqsanger.gz

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CALHM6 is an immunological synapse ion channel required for macrophage-natural killer cell communication upon bacterial infection

Project description:Membrane ion channels of the calcium homeostasis modulator (CALHM) family promote cell-cell crosstalk at synapses via ATP release, where ATP acts as a neurotransmitter. CALHM6, the only CALHM highly expressed in immune cells, has been linked to induction of natural killer (NK) cell anti-tumour activity. Its mechanism of action and broader functions in the immune system are, however, unclear. Here we generated Calhm6-/- mice and report that CALHM6 is important for regulating the early innate control of Listeria monocytogenes infection in vivo. We find that CALHM6 is upregulated in macrophages by pathogen-derived signals, and that it relocates from intracellular compartment to the macrophage-NK cell synapse, facilitating ATP release and controlling the kinetics of NK cell activation. Anti-inflammatory cytokines terminate CALHM6 expression. CALHM6 forms an ion channel when expressed in the plasma membrane of Xenopus oocytes, where channel opening is controlled by a conserved acidic residue, E119, but CALHM6 is localized to intracellular compartments in mammalian cells. Our results contribute to understanding of neurotransmitter-like signal exchange between immune cells that fine-tunes the timing of innate immune responses.

2023-02-01 | GSE223008 | GEO

An integrated workflow for phosphopeptide identification in natural killer cells (NK) and their targets during immunological synapse formation

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2022-11-04 | MSV000090645 | MassIVE

Tumor cells impair immunological synapse formation via central nervous system-enriched metabolite

Project description:Tumor cells impair immunological synapse formation via central nervous system-enriched metabolite

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Tumor cells impair immunological synapse formation via central nervous system-enriched metabolite

Project description:Tumor cells impair immunological synapse formation via central nervous system-enriched metabolite

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Phase separation of chimeric antigen receptor promotes immunological synapse maturation and persistent cytotoxicity

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The ion channel CALHM6 controls bacterial infection-induced cellular cross-talk at the immunological synapse.

Project description:Membrane ion channels of the calcium homeostasis modulator (CALHM) family promote cell-cell crosstalk at neuronal synapses via ATP release, where ATP acts as a neurotransmitter. CALHM6, the only CALHM highly expressed in immune cells, has been linked to the induction of natural killer (NK) cell anti-tumour activity. However, its mechanism of action and broader functions in the immune system remain unclear. Here, we generated Calhm6-/- mice and report that CALHM6 is important for the regulation of the early innate control of Listeria monocytogenes infection in vivo. We find that CALHM6 is upregulated in macrophages by pathogen-derived signals and that it relocates from the intracellular compartment to the macrophage-NK cell synapse, facilitating ATP release and controlling the kinetics of NK cell activation. Anti-inflammatory cytokines terminate CALHM6 expression. CALHM6 forms an ion channel when expressed in the plasma membrane of Xenopus oocytes, where channel opening is controlled by a conserved acidic residue, E119. In mammalian cells, CALHM6 is localised to intracellular compartments. Our results contribute to the understanding of neurotransmitter-like signal exchange between immune cells that fine-tunes the timing of innate immune responses.

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Phase separation of chimeric antigen receptor promotes immunological synapse maturation and persistent cytotoxicity

Project description:Major challenges of CAR-T cell therapy include poor antigen sensitivity and cell persistence. Here we report a solution to these issues by exploiting CAR phase separation. We found that incorporation of an engineered CD3e motif, EB6I, to the conventional 28Z or BBZ CAR induced self-phase separation through cation-π interactions. EB6I CAR can form a mature immunological synapse with CD2 corolla to transduce efficient antigen and costimulatory signaling, while its tonic signaling remains at low levels. Functionally, EB6I CAR-T cells exhibited improved signaling and cytoxicity against low-antigen tumor and persistent tumor killing function. In multiple primary and relapsed murine tumor models, EB6I CAR-T cells exerted better antitumor functions than conventional CAR-T cells against blood and solid cancers. This study thus unveils a new CAR engineering strategy to improve CAR-T cell immunity by leveraging molecular condensation and signaling integration.

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The ion channel CALHM6 controls bacterial infection-induced cellular cross-talk at the immunological synapse

Project description:Membrane ion channels of the calcium homeostasis modulator (CALHM) family promote cell-cell crosstalk at neuronal synapses via ATP release, where ATP acts as a neurotransmitter. CALHM6, the only CALHM highly expressed in immune cells, has been linked to induction of natural killer (NK) cell anti-tumour activity. However, its mechanism of action and broader functions in the immune system remain unclear. Here, we generated Calhm6-/- mice and report that CALHM6 is important for regulation of the early innate control of Listeria monocytogenes infection in vivo. We find that CALHM6 is upregulated in macrophages by pathogen-derived signals, and that it relocates from the intracellular compartment to the macrophage-NK cell synapse, facilitating ATP release and controlling the kinetics of NK cell activation. Anti-inflammatory cytokines terminate CALHM6 expression. CALHM6 forms an ion channel when expressed in the plasma membrane of Xenopus oocytes, where channel opening is controlled by a conserved acidic residue, E119. In mammalian cells, CALHM6 is localized to intracellular compartments. Our results contribute to understanding of neurotransmitter-like signal exchange between immune cells that fine-tunes the timing of innate immune responses.

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Tumor cells impair immunological synapse formation via central nervous system-enriched metabolite

Project description:Tumors employ various strategies to evade immune surveillance. Central nervous system (CNS) has multiple features to restrain immune response，because cranial inflammation can rapidly develop into lethal brain edema. However, whether tumors and CNS share similar programs of immune tolerance is elusive. Here, we analyzed transcriptomic and metabolomic profiles of tumors from patients with HER2+ breast cancer, who received trastuzumab, anti-PD-L1 antibodies and docetaxel (KN035-TH-HER2 study). We found that a neuronal metabolite N-acetylaspartate (NAA) and its synthetase N-acetyltransferase 8-like (NAT8L) are enriched in resistant tumors. In CNS, NAA is released during brain inflammation. We showed that NAT8L attenuates brain inflammation in experimental autoimmune encephalomyelitis (EAE) and impairs anti-tumor immunity by inhibiting cytotoxicity of NK cells and CD8+ T cells via NAA. Mechanistically, NAA disrupts the formation of immunological synapse by inducing K542 acetylation of lamin A, which inhibits the integration between lamin A and SUN2 and consequently impairs polarization of lytic granules in NK cells and CD8+ T cells. Our study uncovered that tumor cells mimic the anti-inflammatory protective barrier of CNS to evade from anti-tumor immunity and NAT8L is a potential target to enhance efficacy of anti-cancer agents

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Ion Channel Expression Patterns in Glioblastoma Stem Cells with Functional and Therapeutic Implications for Malignancy

Project description:Ion channels and transporters have increasingly recognized roles in cancer progression through the regulation of cell proliferation, migration, and death. Glioblastoma stem-like cells (GSCs) are a source of tumor formation and recurrence in glioblastoma multiforme, a highly aggressive brain cancer, suggesting that ion channel expression may be perturbed in this population. However, little is known about the expression and functional relevance of ion channels that may contribute to GSC malignancy. Using RNA sequencing, we assessed the enrichment of ion channels in GSC isolates and non-tumor neural cell types. We identified a unique set of GSC-enriched ion channels using differential expression analysis that stratify by molecular subtype and are associated with distinct gene mutation signatures. In support of potential clinical relevance, expression of selected GSC-enriched ion channels evaluated in human glioblastoma databases of The Cancer Genome Atlas and Ivy Glioblastoma Atlas Project correlated with patient survival times. Finally, genetic knockdown or pharmacological inhibition of individual or classes of GSC-enriched ion channels constrained growth of GSCs compared to normal neural stem cells. This first-in-kind global examination characterizes ion channels enriched in GSCs and explores their potential clinical relevance to glioblastoma molecular subtypes, gene mutations, survival outcomes, regional tumor expression, and experimental responses to loss-of-function. Together, the data support the potential biological and therapeutic impact of ion channels on GSC malignancy and provide strong rationale for further examination of their mechanistic and therapeutic importance.

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