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cells, tim, cancer, esophageal, expression, article, patients, tumor, tnfα, cell, google, scholar, fig, human, cas, tissues, significant, tumorinfiltrating, til, flow, mice, immune, analysis, data, peripheral, immunol, dysfunction, natural, nfκb, microenvironment, pbmc, killer, functions, subsets, healthy, levels, prognosis, inhibitor, exhaustion, blood, ifnγ, cytometry, results, frequency, donors, pathological, poor, lymphocytes, surface, reported,

Topics {✒️}

tumour necrosis factor tumor necrosis factor-α blocking pd-1/pd-l1 signaling suppresses cell-mediated cytotoxicity nf-κb signaling pathway reducing t-cell responses regulating anti-tumor immunity fluorochrome-conjugated primary antibodies translational medicine aims restoring anti-tumor activity t-cell immunoglobulin domain tnf-α mrna levels recombinant human tnf-α 4nqo-induced esophageal lesions cancer-related death worldwide modified gt-t551 medium 4-nqo-induced animal model step qrt-pcr kit tumor-infiltrating nk cells carcinogen-induced esophageal cancer recombinant human tgf-β enhance ifn-γ production article download pdf suppress ifn-γ production quantitative real-time pcr activation-induced inhibitory molecule 5 ng/ml tnf-α added tnf-α inhibitor nf-κb inhibitor cd3−cd56dim nk cells nf-κb pathway determined tnf-α level examined ifn-γ production tnf-α leads relative mrna levels nk cells cultured nf-κb cascade nf-κb mediates blocking tim-3 signaling privacy choices/manage cookies inhibitory molecule expressed cell immunoglobulin domain examined mrna levels squamous cell carcinoma gm-csf article 28 nk cell death human esophageal cancer infiltrating nk cells early research suggests primary esophageal cancer

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WebPage:
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         headline:TNF-α-induced Tim-3 expression marks the dysfunction of infiltrating natural killer cells in human esophageal cancer
         description:Impairment of natural killer (NK) cell activity is an important mechanism of tumor immunoevasion. T cell immunoglobulin domain and mucin domain-3 (Tim-3) is an activation-induced inhibitory molecule, inducing effector lymphocyte exhaustion in chronic viral infection and cancers. However, its function in NK cells in human esophageal cancer remains unclear. We prospectively collected peripheral blood and tumor samples from 53 patients with esophageal cancer. Peripheral and tumor-infiltrating NK cells were analyzed for Tim-3, Annexin V, CD69, CD107a and IFN-γ expression by flow cytometry. Quantitative real-time PCR was used to test relative mRNA expression of IFN-γ, granzyme B, perforin and NKG2D in sorted Tim-3+ NK cells and Tim-3− NK cells, respectively. NK cells isolated from healthy donors were treated with recombinant TNF-α to induce Tim-3 expression. Tim-3 and TNF-α mRNA levels in tumor tissues were measured in both humans and mice. Finally, associations between NK cell frequencies with pathological parameters were investigated. We observed up-regulation of Tim-3 expression on NK cells from esophageal cancer patients, especially at the tumor site. Furthermore, tumor-infiltrating NK cells with high Tim-3 expression exhibited a phenotype with enhanced dysfunction. In vitro, Tim-3 expression on NK cells isolated from blood of healthy donors can be induced by recombinant TNF-α via NF-κB pathway. In both animal models and patients, the Tim-3 level was positively correlated with TNF-α expression in esophageal cancer tissues. Finally, higher Tim-3 level on tumor-infiltrating NK cells is correlated with tumor invasion, nodal status and poor stage in patients with esophageal cancer. Taken together, Tim-3 may play a crucial role to induce NK cell dysfunction in tumor microenvironment and could serve as a potential biomarker for prognosis of esophageal cancer.
         datePublished:2019-05-20T00:00:00Z
         dateModified:2019-05-20T00:00:00Z
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            NK cells
            Tim-3
            TNF-α
            Esophageal cancer
            Biomedicine
            general
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      headline:TNF-α-induced Tim-3 expression marks the dysfunction of infiltrating natural killer cells in human esophageal cancer
      description:Impairment of natural killer (NK) cell activity is an important mechanism of tumor immunoevasion. T cell immunoglobulin domain and mucin domain-3 (Tim-3) is an activation-induced inhibitory molecule, inducing effector lymphocyte exhaustion in chronic viral infection and cancers. However, its function in NK cells in human esophageal cancer remains unclear. We prospectively collected peripheral blood and tumor samples from 53 patients with esophageal cancer. Peripheral and tumor-infiltrating NK cells were analyzed for Tim-3, Annexin V, CD69, CD107a and IFN-γ expression by flow cytometry. Quantitative real-time PCR was used to test relative mRNA expression of IFN-γ, granzyme B, perforin and NKG2D in sorted Tim-3+ NK cells and Tim-3− NK cells, respectively. NK cells isolated from healthy donors were treated with recombinant TNF-α to induce Tim-3 expression. Tim-3 and TNF-α mRNA levels in tumor tissues were measured in both humans and mice. Finally, associations between NK cell frequencies with pathological parameters were investigated. We observed up-regulation of Tim-3 expression on NK cells from esophageal cancer patients, especially at the tumor site. Furthermore, tumor-infiltrating NK cells with high Tim-3 expression exhibited a phenotype with enhanced dysfunction. In vitro, Tim-3 expression on NK cells isolated from blood of healthy donors can be induced by recombinant TNF-α via NF-κB pathway. In both animal models and patients, the Tim-3 level was positively correlated with TNF-α expression in esophageal cancer tissues. Finally, higher Tim-3 level on tumor-infiltrating NK cells is correlated with tumor invasion, nodal status and poor stage in patients with esophageal cancer. Taken together, Tim-3 may play a crucial role to induce NK cell dysfunction in tumor microenvironment and could serve as a potential biomarker for prognosis of esophageal cancer.
      datePublished:2019-05-20T00:00:00Z
      dateModified:2019-05-20T00:00:00Z
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         Tumor microenvironment
         NK cells
         Tim-3
         TNF-α
         Esophageal cancer
         Biomedicine
         general
         Medicine/Public Health
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      name:Biotherapy Center, The First Affiliated Hospital, Zhengzhou University, Zhengzhou, China
      name:Biotherapy Center, The First Affiliated Hospital, Zhengzhou University, Zhengzhou, China
      name:Biotherapy Center, The First Affiliated Hospital, Zhengzhou University, Zhengzhou, China
      name:Department of Thoracic Surgery, The First Affiliated Hospital, Zhengzhou University, Zhengzhou, China
      name:Department of Thoracic Surgery, The First Affiliated Hospital, Zhengzhou University, Zhengzhou, China
      name:Biotherapy Center, The First Affiliated Hospital, Zhengzhou University, Zhengzhou, China
      name:Biotherapy Center, The First Affiliated Hospital, Zhengzhou University, Zhengzhou, China

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