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Tim-3 on natural killer cells regulates immune response via antibody dependent cellular cytotoxicity in HER2-positive gastric cancer

ABSTRACT: Tim-3 on natural killer cells regulates immune response via antibody dependent cellular cytotoxicity in HER2-positive gastric cancer

PROVIDER: PRJNA1068964 | ENA |

REPOSITORIES: ENA

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Tim-3 on natural killer cells regulates immune response via antibody dependent cellular cytotoxicity in HER2-positive gastric cancer

Project description:The present study suggests that combined therapy with anti-Tim-3 antibodies and trastuzumab can be a new treatment strategy for HER2-positive GC.

2024-12-26 | GSE254188 | GEO

NKCLR3 impairs natural killer cell cytotoxicity by epigenetically targeting the Natural Cytotoxicity Triggering Receptor 1 (NCR1) [lncRNA-seq]

Project description:Natural killer cells (NK cells) play a critical role in the surveillance of tumor immunity. However, NK cell-based immunotherapy, including autologous and allogeneic NK cell reinfusion, has not brought significant clinical benefits to patients. To identify factors that control the intrinsic cytotoxicity of NK cells, we utilized the histone deacetylase inhibitor valproic acid (VPA) to develop a NK cell cytotoxicity suppression model. With RNA-seq and functional assays, we identified a previously uncharacterized lncRNA, NKCLR3 (NK cytotoxicity-associated long noncoding RNA 3), as a negative regulatory factor of NK cell-mediated cytotoxicity. NKCLR3 was significantly upregulated in VPA-treated NK cells and was negatively associated with the cytotoxicity of NK cells. Knockdown of NKCLR3 enhanced antitumor activity in NK-92MI cells. Using reverse transcription-associated capture sequencing (RAT-seq), we found that NKCLR3 functioned by targeting the Natural cytotoxicity triggering receptor 1 (NCR1) gene, which encodes the activating receptor NKp46 involved in the natural cytotoxicity. Mechanistic studies revealed that NKCLR3 interacted with the regulatory elements of NCR1 and blocked the formation of an intrachromosomal interaction that is required for optimal expression of NCR1. In addition, NKCLR3 inhibited the synthesis of NCR1 enhancer RNA. Through these dual mechanisms, NKCLR3 induced a suppressive epigenotype in the NCR1 promoter and suppressed the expression of the NCR1 gene. Thus, the NKCLR3-NCR1 axis identified in this study may serve as a novel target to improve therapeutic intervention of NK cells in tumor immunotherapy.

2025-01-01 | GSE285271 | GEO

NKCLR3 impairs natural killer cell cytotoxicity by epigenetically targeting the Natural Cytotoxicity Triggering Receptor 1 (NCR1)

Project description:NKCLR3 impairs natural killer cell cytotoxicity by epigenetically targeting the Natural Cytotoxicity Triggering Receptor 1 (NCR1)

| PRJNA1200109 | ENA

CHMP2A regulates tumor sensitivity to natural killer cell-mediated cytotoxicity

Project description:CHMP2A regulates tumor sensitivity to natural killer cell-mediated cytotoxicity

| PRJNA734153 | ENA

NKCLR3 impairs natural killer cell cytotoxicity by epigenetically targeting the Natural Cytotoxicity Triggering Receptor 1 (NCR1) [lncRNA-seq]

Project description:NKCLR3 impairs natural killer cell cytotoxicity by epigenetically targeting the Natural Cytotoxicity Triggering Receptor 1 (NCR1) [lncRNA-seq]

| PRJNA1202133 | ENA

CHMP2A regulates tumor sensitivity to natural killer cell-mediated cytotoxicity [CRISPR]

Project description:CHMP2A regulates tumor sensitivity to natural killer cell-mediated cytotoxicity [CRISPR]

| PRJNA734155 | ENA

NKCLR3 impairs natural killer cell cytotoxicity by epigenetically targeting the Natural Cytotoxicity Triggering Receptor 1 (NCR1)

Project description:RNA-Seq reveals that NKCLR3 (NK cytotoxicity-associated long noncoding RNA 3, NONHSAT026854) is differentially expressed in VPA-treated human NK cells. To determine whether it is functionally important in NK cell cytotoxicity, we used a RNA reverse transcription-associated trap sequencing (RAT-Seq) approach to profile the genome-wide binding targets for NKCLR3. This dataset will help study the mechanisms underlying the role of NKCLR3 in NK cell cytotoxicity.

2025-01-01 | GSE284721 | GEO

CHMP2A regulates tumor sensitivity to natural killer cell-mediated cytotoxicity [RNA-seq]

Project description:CHMP2A regulates tumor sensitivity to natural killer cell-mediated cytotoxicity [RNA-seq]

| PRJNA734156 | ENA

Novel non-canonical role of STAT1 in Natural Killer cell cytotoxicity

Project description:STAT1 is an important regulator of NK cell maturation and cytotoxicity. Although the consequences of Stat1-deficiency have been described in detail the underlying molecular functions of STAT1 in NK cells are only partially understood. Here we describe a novel non-canonical role of STAT1 that was unmasked in NK cells expressing Stat1-Y701F. This mutation prevents JAK-dependent phosphorylation, subsequent nuclear translocation and cytokine-induced transcriptional activity. As expected Stat1-Y701F mice displayed impaired NK cell maturation comparable to Stat1-/- animals. In contrast Stat1-Y701F NK cells exerted a significantly enhanced cytotoxicity in vitro and in vivo suggesting a so-far unknown cytoplasmic function. Using immunofluorescence technology we uncovered the recruitment of STAT1 to the immunological synapse during NK cell killing. A Stat1ind mouse expressing FLAG-tagged STAT1α was used to study the STAT1α interactome in NK cells. Mass spectrometry revealed that STAT1 directly binds proteins involved in cell junction formation and proteins associated to membrane or membrane-bound vesicles. We propose a novel function for STAT1 in the immunological synapse of NK cells regulating tumor surveillance and cytotoxicity.

2016-10-07 | PXD002206 | Pride

Tim-3 marks human natural killer cell maturation and suppresses cell-mediated cytotoxicity.

Project description:Natural killer (NK) cells are innate lymphocytes that play an important role against viral infections and cancer. This effect is achieved through a complex mosaic of inhibitory and activating receptors expressed by NK cells that ultimately determine the magnitude of the NK-cell response. The T-cell immunoglobulin- and mucin domain-containing (Tim)-3 receptor was initially identified as a T-helper 1-specific type I membrane protein involved in regulating T-cell responses. Human NK cells transcribe the highest amounts of Tim-3 among lymphocytes. Tim-3 protein is expressed on essentially all mature CD56(dim)CD16(+) NK cells and is expressed heterogeneously in the immature CD56(bright)CD16(-) NK-cell subset in blood from healthy adults and in cord blood. Tim-3 expression was induced on CD56(bright)CD16(-) NK cells after stimulation with IL-15 or IL-12 and IL-18 in vitro, suggesting that Tim-3 is a maturation marker on NK cells. Whereas Tim-3 has been used to identify dysfunctional T cells, NK cells expressing high amounts of Tim-3 are fully responsive with respect to cytokine production and cytotoxicity. However, when Tim-3 was cross-linked with antibodies it suppressed NK cell-mediated cytotoxicity. These findings suggest that NK-cell responses may be negatively regulated when NK cells encounter target cells expressing cognate ligands of Tim-3.

| S-EPMC3335380 | biostudies-literature

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