DOI . ORG {
}
We began analyzing https://link.springer.com/article/10.1007/s10555-007-9054-2, but it redirected us to https://link.springer.com/article/10.1007/s10555-007-9054-2. The analysis below is for the second page.
Title[redir]:
Hypoxia-dependent anti-inflammatory pathways in protection of cancerous tissues | Cancer and Metastasis Reviews
Description:
The evolutionarily selected tissue-protecting mechanisms are likely to be triggered by an event of universal significance for all surrounding cells. Such an event could be damage to blood vessels, which would result in local tissue hypoxia. It is now recognized that tissue hypoxia can initiate the tissue-protecting mechanism mediated by at least two different biochemical pathways. The central message of this review is that tumor cells are protected from immune damage in hypoxic and immunosuppressive tumor microenvironments due to the inactivation of anti-tumor T cells by the combined action of these two hypoxia-driven mechanisms. Firstly, tumor hypoxia-produced extracellular adenosine inhibits anti-tumor T cells via their Gs-protein-coupled and cAMP-elevating A2A and A2B adenosine receptors (A2AR/A2BR). Levels of extracellular adenosine are increased in tumor microenvironments due to the changes in activities of enzymes involved in adenosine metabolism. Secondly, TCR-activated and/or tumor hypoxia-exposed anti-tumor T cells may be inhibited in tumor microenvironments by Hypoxia-inducible Factor 1α (HIF-1α) Hence, HIF-1α activity in T cells may contribute to the tumor-protecting immunosuppressive effects of tumor hypoxia. Here, we summarize the data that support the view that protection of hypoxic cancerous tissues from anti-tumor T cells is mediated by the same mechanism that protects normal tissues from the excessive collateral damage by overactive immune cells during acute inflammation.
Title[redir]:
Hypoxia-dependent anti-inflammatory pathways in protection of cancerous tissues | Cancer and Metastasis Reviews
Description:
The evolutionarily selected tissue-protecting mechanisms are likely to be triggered by an event of universal significance for all surrounding cells. Such an event could be damage to blood vessels, which would result in local tissue hypoxia. It is now recognized that tissue hypoxia can initiate the tissue-protecting mechanism mediated by at least two different biochemical pathways. The central message of this review is that tumor cells are protected from immune damage in hypoxic and immunosuppressive tumor microenvironments due to the inactivation of anti-tumor T cells by the combined action of these two hypoxia-driven mechanisms. Firstly, tumor hypoxia-produced extracellular adenosine inhibits anti-tumor T cells via their Gs-protein-coupled and cAMP-elevating A2A and A2B adenosine receptors (A2AR/A2BR). Levels of extracellular adenosine are increased in tumor microenvironments due to the changes in activities of enzymes involved in adenosine metabolism. Secondly, TCR-activated and/or tumor hypoxia-exposed anti-tumor T cells may be inhibited in tumor microenvironments by Hypoxia-inducible Factor 1α (HIF-1α) Hence, HIF-1α activity in T cells may contribute to the tumor-protecting immunosuppressive effects of tumor hypoxia. Here, we summarize the data that support the view that protection of hypoxic cancerous tissues from anti-tumor T cells is mediated by the same mechanism that protects normal tissues from the excessive collateral damage by overactive immune cells during acute inflammation.
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Keywords {🔍}
google, scholar, cas, pubmed, article, cancer, adenosine, journal, cells, immunology, cell, sitkovsky, tumor, research, factor, immunotherapy, hypoxia, lukashev, ohta, reviews, hypoxiainducible, role, human, immune, nature, protection, mechanisms, review, receptors, molecular, tissue, antitumor, inflammation, tumors, receptor, clinical, content, extracellular, development, tumour, regulation, apasov, annual, pharmacology, caldwell, biological, kinase, alpha, lymphocytes, privacy,
Topics {✒️}
hypoxia-dependent anti-inflammatory pathways tumor-induced l-selectinhigh suppressor tumor hypoxia-exposed anti-tumor g-protein-coupled adenosine receptors month download article/chapter hypoxia-inducible factor 1α hypoxia-inducible factor-1 alpha hypoxia-inducible factor 1alpha hypoxia-inducible factor 1a camp-dependent protein kinase activation-inducible short isoform targeting tumor-related immunosuppression cd39/vascular atp diphosphohydrolase phosphatidylinositol 3-kinase-mediated pathways high-resolution measurements reveal adenosine receptor-mediated mechanisms ecto-atp diphosphohydrolase/cd39 regulatory t-cell-inactivation tumor-protecting immunosuppressive effects hypoxia-inducible factor 1 shape tumour immunogenicity gs-protein-coupled tissue-protecting mechanism mediated hypoxia-driven mechanisms cell-based cancer immunotherapy van der burg hypoxia-inducible factors myeloid cell-mediated inflammation ecto-nucleotidases-molecular structures physiological tissue-protecting mechanism local-tissue oxygen tension t-cell recognition full article pdf endogenous adenosine produced cytotoxic t-lymphocytes receptor-mediated mechanisms significant compensatory increases key regulatory factor tumour growth camp-elevating a2a adenosine a2a receptors malignant melanoma ascites privacy choices/manage cookies hif-1α activity local tissue hypoxia metastasis reviews aims tumor microenvironments due inflammatory tissue damage drug discovery today hypoxia-induced inhibition
Questions {❓}
- The ‘danger’ sensors that STOP the immune response: The A2 adenosine receptors?
Schema {🗺️}
WebPage:
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headline:Hypoxia-dependent anti-inflammatory pathways in protection of cancerous tissues
description:The evolutionarily selected tissue-protecting mechanisms are likely to be triggered by an event of universal significance for all surrounding cells. Such an event could be damage to blood vessels, which would result in local tissue hypoxia. It is now recognized that tissue hypoxia can initiate the tissue-protecting mechanism mediated by at least two different biochemical pathways. The central message of this review is that tumor cells are protected from immune damage in hypoxic and immunosuppressive tumor microenvironments due to the inactivation of anti-tumor T cells by the combined action of these two hypoxia-driven mechanisms. Firstly, tumor hypoxia-produced extracellular adenosine inhibits anti-tumor T cells via their Gs-protein-coupled and cAMP-elevating A2A and A2B adenosine receptors (A2AR/A2BR). Levels of extracellular adenosine are increased in tumor microenvironments due to the changes in activities of enzymes involved in adenosine metabolism. Secondly, TCR-activated and/or tumor hypoxia-exposed anti-tumor T cells may be inhibited in tumor microenvironments by Hypoxia-inducible Factor 1α (HIF-1α) Hence, HIF-1α activity in T cells may contribute to the tumor-protecting immunosuppressive effects of tumor hypoxia. Here, we summarize the data that support the view that protection of hypoxic cancerous tissues from anti-tumor T cells is mediated by the same mechanism that protects normal tissues from the excessive collateral damage by overactive immune cells during acute inflammation.
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headline:Hypoxia-dependent anti-inflammatory pathways in protection of cancerous tissues
description:The evolutionarily selected tissue-protecting mechanisms are likely to be triggered by an event of universal significance for all surrounding cells. Such an event could be damage to blood vessels, which would result in local tissue hypoxia. It is now recognized that tissue hypoxia can initiate the tissue-protecting mechanism mediated by at least two different biochemical pathways. The central message of this review is that tumor cells are protected from immune damage in hypoxic and immunosuppressive tumor microenvironments due to the inactivation of anti-tumor T cells by the combined action of these two hypoxia-driven mechanisms. Firstly, tumor hypoxia-produced extracellular adenosine inhibits anti-tumor T cells via their Gs-protein-coupled and cAMP-elevating A2A and A2B adenosine receptors (A2AR/A2BR). Levels of extracellular adenosine are increased in tumor microenvironments due to the changes in activities of enzymes involved in adenosine metabolism. Secondly, TCR-activated and/or tumor hypoxia-exposed anti-tumor T cells may be inhibited in tumor microenvironments by Hypoxia-inducible Factor 1α (HIF-1α) Hence, HIF-1α activity in T cells may contribute to the tumor-protecting immunosuppressive effects of tumor hypoxia. Here, we summarize the data that support the view that protection of hypoxic cancerous tissues from anti-tumor T cells is mediated by the same mechanism that protects normal tissues from the excessive collateral damage by overactive immune cells during acute inflammation.
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